Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities
The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic...
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| Autor*in: |
Tuleta, Izabela [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2021transfer abstract |
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| Übergeordnetes Werk: |
Enthalten in: Parents’ ambitions and children’s competitiveness - Khadjavi, Menusch ELSEVIER, 2018, Amsterdam [u.a.] |
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| Übergeordnetes Werk: |
volume:176 ; year:2021 ; pages:0 |
| Links: |
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| DOI / URN: |
10.1016/j.addr.2021.113904 |
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ELV055229808 |
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| 520 | |a The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. | ||
| 520 | |a The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. | ||
| 650 | 7 | |a Heart failure |2 Elsevier | |
| 650 | 7 | |a Oxidative stress |2 Elsevier | |
| 650 | 7 | |a Hyperglycemia |2 Elsevier | |
| 650 | 7 | |a Fibrosis |2 Elsevier | |
| 650 | 7 | |a Inflammation |2 Elsevier | |
| 650 | 7 | |a Diabetes |2 Elsevier | |
| 650 | 7 | |a Glucose-lowering agents |2 Elsevier | |
| 650 | 7 | |a Lipotoxicity |2 Elsevier | |
| 650 | 7 | |a Fibroblast |2 Elsevier | |
| 700 | 1 | |a Frangogiannis, Nikolaos G. |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Khadjavi, Menusch ELSEVIER |t Parents’ ambitions and children’s competitiveness |d 2018 |g Amsterdam [u.a.] |w (DE-627)ELV000099058 |
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10.1016/j.addr.2021.113904 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001874.pica (DE-627)ELV055229808 (ELSEVIER)S0169-409X(21)00297-0 DE-627 ger DE-627 rakwb eng 150 300 330 VZ 77.00 bkl Tuleta, Izabela verfasserin aut Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. Heart failure Elsevier Oxidative stress Elsevier Hyperglycemia Elsevier Fibrosis Elsevier Inflammation Elsevier Diabetes Elsevier Glucose-lowering agents Elsevier Lipotoxicity Elsevier Fibroblast Elsevier Frangogiannis, Nikolaos G. oth Enthalten in Elsevier Science Khadjavi, Menusch ELSEVIER Parents’ ambitions and children’s competitiveness 2018 Amsterdam [u.a.] (DE-627)ELV000099058 volume:176 year:2021 pages:0 https://doi.org/10.1016/j.addr.2021.113904 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 77.00 Psychologie: Allgemeines VZ AR 176 2021 0 |
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10.1016/j.addr.2021.113904 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001874.pica (DE-627)ELV055229808 (ELSEVIER)S0169-409X(21)00297-0 DE-627 ger DE-627 rakwb eng 150 300 330 VZ 77.00 bkl Tuleta, Izabela verfasserin aut Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. Heart failure Elsevier Oxidative stress Elsevier Hyperglycemia Elsevier Fibrosis Elsevier Inflammation Elsevier Diabetes Elsevier Glucose-lowering agents Elsevier Lipotoxicity Elsevier Fibroblast Elsevier Frangogiannis, Nikolaos G. oth Enthalten in Elsevier Science Khadjavi, Menusch ELSEVIER Parents’ ambitions and children’s competitiveness 2018 Amsterdam [u.a.] (DE-627)ELV000099058 volume:176 year:2021 pages:0 https://doi.org/10.1016/j.addr.2021.113904 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 77.00 Psychologie: Allgemeines VZ AR 176 2021 0 |
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10.1016/j.addr.2021.113904 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001874.pica (DE-627)ELV055229808 (ELSEVIER)S0169-409X(21)00297-0 DE-627 ger DE-627 rakwb eng 150 300 330 VZ 77.00 bkl Tuleta, Izabela verfasserin aut Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. Heart failure Elsevier Oxidative stress Elsevier Hyperglycemia Elsevier Fibrosis Elsevier Inflammation Elsevier Diabetes Elsevier Glucose-lowering agents Elsevier Lipotoxicity Elsevier Fibroblast Elsevier Frangogiannis, Nikolaos G. oth Enthalten in Elsevier Science Khadjavi, Menusch ELSEVIER Parents’ ambitions and children’s competitiveness 2018 Amsterdam [u.a.] (DE-627)ELV000099058 volume:176 year:2021 pages:0 https://doi.org/10.1016/j.addr.2021.113904 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 77.00 Psychologie: Allgemeines VZ AR 176 2021 0 |
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10.1016/j.addr.2021.113904 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001874.pica (DE-627)ELV055229808 (ELSEVIER)S0169-409X(21)00297-0 DE-627 ger DE-627 rakwb eng 150 300 330 VZ 77.00 bkl Tuleta, Izabela verfasserin aut Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. Heart failure Elsevier Oxidative stress Elsevier Hyperglycemia Elsevier Fibrosis Elsevier Inflammation Elsevier Diabetes Elsevier Glucose-lowering agents Elsevier Lipotoxicity Elsevier Fibroblast Elsevier Frangogiannis, Nikolaos G. oth Enthalten in Elsevier Science Khadjavi, Menusch ELSEVIER Parents’ ambitions and children’s competitiveness 2018 Amsterdam [u.a.] (DE-627)ELV000099058 volume:176 year:2021 pages:0 https://doi.org/10.1016/j.addr.2021.113904 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 77.00 Psychologie: Allgemeines VZ AR 176 2021 0 |
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10.1016/j.addr.2021.113904 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001874.pica (DE-627)ELV055229808 (ELSEVIER)S0169-409X(21)00297-0 DE-627 ger DE-627 rakwb eng 150 300 330 VZ 77.00 bkl Tuleta, Izabela verfasserin aut Fibrosis of the diabetic heart: Clinical significance, molecular mechanisms, and therapeutic opportunities 2021transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. Heart failure Elsevier Oxidative stress Elsevier Hyperglycemia Elsevier Fibrosis Elsevier Inflammation Elsevier Diabetes Elsevier Glucose-lowering agents Elsevier Lipotoxicity Elsevier Fibroblast Elsevier Frangogiannis, Nikolaos G. oth Enthalten in Elsevier Science Khadjavi, Menusch ELSEVIER Parents’ ambitions and children’s competitiveness 2018 Amsterdam [u.a.] (DE-627)ELV000099058 volume:176 year:2021 pages:0 https://doi.org/10.1016/j.addr.2021.113904 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 77.00 Psychologie: Allgemeines VZ AR 176 2021 0 |
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The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. |
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The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. |
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The cell biology of diabetic cardiac fibrosis. The primary metabolic perturbations of type 1 and type 2 diabetes, hypeglycemia and insulin resistance, activate cardiac fibroblasts, the main cellular effectors of cardiac fibrosis. In addition to their direct effects on cardiac fibroblasts, metabolic changes may promote fibrosis through actions on other myocardial cell types, such as cardiomyocytes, immune cells and vascular cells. In the diabetic heart, cardiomyocytes may exhibit activation of oxidative pathways, resulting in release of fibrogenic cytokines and growth factors, and local activation of angiotensin II. Inflammatory stimulation may also induce Transforming Growth Factor-β (TGF-β) synthesis by cardiac macrophages and lymphocytes, whereas mast cells may secrete chymase, activating an alternative pathway involved in angiotensin II generation. Endothelial cells may contribute to the fibrotic response by producing fibrogenic growth factors and endothelin-1 (ET-1). In the diabetic heart, macrophages, vascular cells and fibroblasts may produce specialized matrix proteins with fibrogenic properties (such as fibronectin (FN) and thrombospondin-1 (TSP-1)). Although resident cardiac fibroblasts are the predominant matrix-producing cells in diabetic hearts, contributions of endothelial cells converting to fibroblasts through endothelial to mesenchymal transition (EndMT), and of mural cells that may acquire a fibroblast phenotype, have been suggested, but not convincingly documented. Increased deposition of interstitial and perivascular collagens and matrix crosslinking, increase myocardial stiffness and may play an important role in development of diastolic dysfunction, and in the pathogenesis of diabetes-associated heart failure with preserved ejection fraction (HFpEF). IL-1 = interleukin-1, ROS = reactive oxygen species, TNF-α = tumor necrosis factor-α. |
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