Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease
Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways hav...
Ausführliche Beschreibung
Autor*in: |
Hoyul Lee [verfasserIn] Jae-Han Jeon [verfasserIn] Eun Soo Kim [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
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2023 |
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Übergeordnetes Werk: |
In: Frontiers in Immunology - Frontiers Media S.A., 2011, 14(2023) |
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Übergeordnetes Werk: |
volume:14 ; year:2023 |
Links: |
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DOI / URN: |
10.3389/fimmu.2023.1219422 |
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DOAJ095099549 |
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10.3389/fimmu.2023.1219422 doi (DE-627)DOAJ095099549 (DE-599)DOAJ497ad25f299f4dec871dd50f183a2318 DE-627 ger DE-627 rakwb eng RC581-607 Hoyul Lee verfasserin aut Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways have been shown to play a crucial role in the metabolic reprogramming of colitogenic T cells, leading to increased inflammatory cytokine production and tissue damage. In addition to metabolic reprogramming, mitochondrial dysfunction has also been implicated in the pathogenesis of IBD. Studies have shown that colitogenic T cells exhibit impaired mitochondrial respiration, elevated levels of mROS, alterations in calcium homeostasis, impaired mitochondrial biogenesis, and aberrant mitochondria-associated membrane formation. Here, we discuss our current knowledge of the metabolic reprogramming and mitochondrial dysfunctions in colitogenic T cells, as well as the potential therapeutic applications for treating IBD with evidence from animal experiments. mitochondria IBD - inflammatory bowel disease immunometabolism T cell treatment inflammation Immunologic diseases. Allergy Jae-Han Jeon verfasserin aut Jae-Han Jeon verfasserin aut Eun Soo Kim verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 14(2023) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:14 year:2023 https://doi.org/10.3389/fimmu.2023.1219422 kostenfrei https://doaj.org/article/497ad25f299f4dec871dd50f183a2318 kostenfrei https://www.frontiersin.org/articles/10.3389/fimmu.2023.1219422/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2023 |
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10.3389/fimmu.2023.1219422 doi (DE-627)DOAJ095099549 (DE-599)DOAJ497ad25f299f4dec871dd50f183a2318 DE-627 ger DE-627 rakwb eng RC581-607 Hoyul Lee verfasserin aut Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways have been shown to play a crucial role in the metabolic reprogramming of colitogenic T cells, leading to increased inflammatory cytokine production and tissue damage. In addition to metabolic reprogramming, mitochondrial dysfunction has also been implicated in the pathogenesis of IBD. Studies have shown that colitogenic T cells exhibit impaired mitochondrial respiration, elevated levels of mROS, alterations in calcium homeostasis, impaired mitochondrial biogenesis, and aberrant mitochondria-associated membrane formation. Here, we discuss our current knowledge of the metabolic reprogramming and mitochondrial dysfunctions in colitogenic T cells, as well as the potential therapeutic applications for treating IBD with evidence from animal experiments. mitochondria IBD - inflammatory bowel disease immunometabolism T cell treatment inflammation Immunologic diseases. Allergy Jae-Han Jeon verfasserin aut Jae-Han Jeon verfasserin aut Eun Soo Kim verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 14(2023) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:14 year:2023 https://doi.org/10.3389/fimmu.2023.1219422 kostenfrei https://doaj.org/article/497ad25f299f4dec871dd50f183a2318 kostenfrei https://www.frontiersin.org/articles/10.3389/fimmu.2023.1219422/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2023 |
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10.3389/fimmu.2023.1219422 doi (DE-627)DOAJ095099549 (DE-599)DOAJ497ad25f299f4dec871dd50f183a2318 DE-627 ger DE-627 rakwb eng RC581-607 Hoyul Lee verfasserin aut Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways have been shown to play a crucial role in the metabolic reprogramming of colitogenic T cells, leading to increased inflammatory cytokine production and tissue damage. In addition to metabolic reprogramming, mitochondrial dysfunction has also been implicated in the pathogenesis of IBD. Studies have shown that colitogenic T cells exhibit impaired mitochondrial respiration, elevated levels of mROS, alterations in calcium homeostasis, impaired mitochondrial biogenesis, and aberrant mitochondria-associated membrane formation. Here, we discuss our current knowledge of the metabolic reprogramming and mitochondrial dysfunctions in colitogenic T cells, as well as the potential therapeutic applications for treating IBD with evidence from animal experiments. mitochondria IBD - inflammatory bowel disease immunometabolism T cell treatment inflammation Immunologic diseases. Allergy Jae-Han Jeon verfasserin aut Jae-Han Jeon verfasserin aut Eun Soo Kim verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 14(2023) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:14 year:2023 https://doi.org/10.3389/fimmu.2023.1219422 kostenfrei https://doaj.org/article/497ad25f299f4dec871dd50f183a2318 kostenfrei https://www.frontiersin.org/articles/10.3389/fimmu.2023.1219422/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2023 |
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10.3389/fimmu.2023.1219422 doi (DE-627)DOAJ095099549 (DE-599)DOAJ497ad25f299f4dec871dd50f183a2318 DE-627 ger DE-627 rakwb eng RC581-607 Hoyul Lee verfasserin aut Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways have been shown to play a crucial role in the metabolic reprogramming of colitogenic T cells, leading to increased inflammatory cytokine production and tissue damage. In addition to metabolic reprogramming, mitochondrial dysfunction has also been implicated in the pathogenesis of IBD. Studies have shown that colitogenic T cells exhibit impaired mitochondrial respiration, elevated levels of mROS, alterations in calcium homeostasis, impaired mitochondrial biogenesis, and aberrant mitochondria-associated membrane formation. Here, we discuss our current knowledge of the metabolic reprogramming and mitochondrial dysfunctions in colitogenic T cells, as well as the potential therapeutic applications for treating IBD with evidence from animal experiments. mitochondria IBD - inflammatory bowel disease immunometabolism T cell treatment inflammation Immunologic diseases. Allergy Jae-Han Jeon verfasserin aut Jae-Han Jeon verfasserin aut Eun Soo Kim verfasserin aut In Frontiers in Immunology Frontiers Media S.A., 2011 14(2023) (DE-627)657998354 (DE-600)2606827-8 16643224 nnns volume:14 year:2023 https://doi.org/10.3389/fimmu.2023.1219422 kostenfrei https://doaj.org/article/497ad25f299f4dec871dd50f183a2318 kostenfrei https://www.frontiersin.org/articles/10.3389/fimmu.2023.1219422/full kostenfrei https://doaj.org/toc/1664-3224 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 14 2023 |
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Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease |
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Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways have been shown to play a crucial role in the metabolic reprogramming of colitogenic T cells, leading to increased inflammatory cytokine production and tissue damage. In addition to metabolic reprogramming, mitochondrial dysfunction has also been implicated in the pathogenesis of IBD. Studies have shown that colitogenic T cells exhibit impaired mitochondrial respiration, elevated levels of mROS, alterations in calcium homeostasis, impaired mitochondrial biogenesis, and aberrant mitochondria-associated membrane formation. Here, we discuss our current knowledge of the metabolic reprogramming and mitochondrial dysfunctions in colitogenic T cells, as well as the potential therapeutic applications for treating IBD with evidence from animal experiments. |
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Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways have been shown to play a crucial role in the metabolic reprogramming of colitogenic T cells, leading to increased inflammatory cytokine production and tissue damage. In addition to metabolic reprogramming, mitochondrial dysfunction has also been implicated in the pathogenesis of IBD. Studies have shown that colitogenic T cells exhibit impaired mitochondrial respiration, elevated levels of mROS, alterations in calcium homeostasis, impaired mitochondrial biogenesis, and aberrant mitochondria-associated membrane formation. Here, we discuss our current knowledge of the metabolic reprogramming and mitochondrial dysfunctions in colitogenic T cells, as well as the potential therapeutic applications for treating IBD with evidence from animal experiments. |
abstract_unstemmed |
Mitochondria has emerged as a critical ruler of metabolic reprogramming in immune responses and inflammation. In the context of colitogenic T cells and IBD, there has been increasing research interest in the metabolic pathways of glycolysis, pyruvate oxidation, and glutaminolysis. These pathways have been shown to play a crucial role in the metabolic reprogramming of colitogenic T cells, leading to increased inflammatory cytokine production and tissue damage. In addition to metabolic reprogramming, mitochondrial dysfunction has also been implicated in the pathogenesis of IBD. Studies have shown that colitogenic T cells exhibit impaired mitochondrial respiration, elevated levels of mROS, alterations in calcium homeostasis, impaired mitochondrial biogenesis, and aberrant mitochondria-associated membrane formation. Here, we discuss our current knowledge of the metabolic reprogramming and mitochondrial dysfunctions in colitogenic T cells, as well as the potential therapeutic applications for treating IBD with evidence from animal experiments. |
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Mitochondrial dysfunctions in T cells: focus on inflammatory bowel disease |
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score |
7.3989124 |