AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model

Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induce...
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Autor*in:	Yang, Chen [verfasserIn] Su, Hong-yong An, Ning Wu, Hong-luan Guo, Xiao-yan Li, Zhi-hang Chen, Xiao-cui Zhu, Shao-ping Wu, Dan Li, Hui-yuan Pan, Qing-jun Liang, Dong Liu, Hua-feng

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2022

Schlagwörter:	Hyperuricemia Renal inflammation Renal fibrosis Urate deposition AMPK α2

Anmerkung:	© The Author(s) 2022

Übergeordnetes Werk:	Enthalten in: European journal of medical research - London : BioMed Central, 2000, 27(2022), 1 vom: 10. Sept.
Übergeordnetes Werk:	volume:27 ; year:2022 ; number:1 ; day:10 ; month:09

Links:	Volltext

DOI / URN:	10.1186/s40001-022-00800-1

Katalog-ID:	SPR050982966

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520			\|a Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney.
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allfields	10.1186/s40001-022-00800-1 doi (DE-627)SPR050982966 (SPR)s40001-022-00800-1-e DE-627 ger DE-627 rakwb eng Yang, Chen verfasserin aut AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney. Hyperuricemia (dpeaa)DE-He213 Renal inflammation (dpeaa)DE-He213 Renal fibrosis (dpeaa)DE-He213 Urate deposition (dpeaa)DE-He213 AMPK α2 (dpeaa)DE-He213 Su, Hong-yong aut An, Ning aut Wu, Hong-luan aut Guo, Xiao-yan aut Li, Zhi-hang aut Chen, Xiao-cui aut Zhu, Shao-ping aut Wu, Dan aut Li, Hui-yuan aut Pan, Qing-jun aut Liang, Dong aut Liu, Hua-feng (orcid)0000-0002-5177-0334 aut Enthalten in European journal of medical research London : BioMed Central, 2000 27(2022), 1 vom: 10. Sept. (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:27 year:2022 number:1 day:10 month:09 https://dx.doi.org/10.1186/s40001-022-00800-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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 27 2022 1 10 09
spelling	10.1186/s40001-022-00800-1 doi (DE-627)SPR050982966 (SPR)s40001-022-00800-1-e DE-627 ger DE-627 rakwb eng Yang, Chen verfasserin aut AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney. Hyperuricemia (dpeaa)DE-He213 Renal inflammation (dpeaa)DE-He213 Renal fibrosis (dpeaa)DE-He213 Urate deposition (dpeaa)DE-He213 AMPK α2 (dpeaa)DE-He213 Su, Hong-yong aut An, Ning aut Wu, Hong-luan aut Guo, Xiao-yan aut Li, Zhi-hang aut Chen, Xiao-cui aut Zhu, Shao-ping aut Wu, Dan aut Li, Hui-yuan aut Pan, Qing-jun aut Liang, Dong aut Liu, Hua-feng (orcid)0000-0002-5177-0334 aut Enthalten in European journal of medical research London : BioMed Central, 2000 27(2022), 1 vom: 10. Sept. (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:27 year:2022 number:1 day:10 month:09 https://dx.doi.org/10.1186/s40001-022-00800-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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 27 2022 1 10 09
allfields_unstemmed	10.1186/s40001-022-00800-1 doi (DE-627)SPR050982966 (SPR)s40001-022-00800-1-e DE-627 ger DE-627 rakwb eng Yang, Chen verfasserin aut AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney. Hyperuricemia (dpeaa)DE-He213 Renal inflammation (dpeaa)DE-He213 Renal fibrosis (dpeaa)DE-He213 Urate deposition (dpeaa)DE-He213 AMPK α2 (dpeaa)DE-He213 Su, Hong-yong aut An, Ning aut Wu, Hong-luan aut Guo, Xiao-yan aut Li, Zhi-hang aut Chen, Xiao-cui aut Zhu, Shao-ping aut Wu, Dan aut Li, Hui-yuan aut Pan, Qing-jun aut Liang, Dong aut Liu, Hua-feng (orcid)0000-0002-5177-0334 aut Enthalten in European journal of medical research London : BioMed Central, 2000 27(2022), 1 vom: 10. Sept. (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:27 year:2022 number:1 day:10 month:09 https://dx.doi.org/10.1186/s40001-022-00800-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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 27 2022 1 10 09
allfieldsGer	10.1186/s40001-022-00800-1 doi (DE-627)SPR050982966 (SPR)s40001-022-00800-1-e DE-627 ger DE-627 rakwb eng Yang, Chen verfasserin aut AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney. Hyperuricemia (dpeaa)DE-He213 Renal inflammation (dpeaa)DE-He213 Renal fibrosis (dpeaa)DE-He213 Urate deposition (dpeaa)DE-He213 AMPK α2 (dpeaa)DE-He213 Su, Hong-yong aut An, Ning aut Wu, Hong-luan aut Guo, Xiao-yan aut Li, Zhi-hang aut Chen, Xiao-cui aut Zhu, Shao-ping aut Wu, Dan aut Li, Hui-yuan aut Pan, Qing-jun aut Liang, Dong aut Liu, Hua-feng (orcid)0000-0002-5177-0334 aut Enthalten in European journal of medical research London : BioMed Central, 2000 27(2022), 1 vom: 10. Sept. (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:27 year:2022 number:1 day:10 month:09 https://dx.doi.org/10.1186/s40001-022-00800-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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 27 2022 1 10 09
allfieldsSound	10.1186/s40001-022-00800-1 doi (DE-627)SPR050982966 (SPR)s40001-022-00800-1-e DE-627 ger DE-627 rakwb eng Yang, Chen verfasserin aut AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2022 Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney. Hyperuricemia (dpeaa)DE-He213 Renal inflammation (dpeaa)DE-He213 Renal fibrosis (dpeaa)DE-He213 Urate deposition (dpeaa)DE-He213 AMPK α2 (dpeaa)DE-He213 Su, Hong-yong aut An, Ning aut Wu, Hong-luan aut Guo, Xiao-yan aut Li, Zhi-hang aut Chen, Xiao-cui aut Zhu, Shao-ping aut Wu, Dan aut Li, Hui-yuan aut Pan, Qing-jun aut Liang, Dong aut Liu, Hua-feng (orcid)0000-0002-5177-0334 aut Enthalten in European journal of medical research London : BioMed Central, 2000 27(2022), 1 vom: 10. Sept. (DE-627)375977775 (DE-600)2129989-4 2047-783X nnns volume:27 year:2022 number:1 day:10 month:09 https://dx.doi.org/10.1186/s40001-022-00800-1 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER 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 27 2022 1 10 09
language	English
source	Enthalten in European journal of medical research 27(2022), 1 vom: 10. Sept. volume:27 year:2022 number:1 day:10 month:09
sourceStr	Enthalten in European journal of medical research 27(2022), 1 vom: 10. Sept. volume:27 year:2022 number:1 day:10 month:09
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Hyperuricemia Renal inflammation Renal fibrosis Urate deposition AMPK α2
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container_title	European journal of medical research
authorswithroles_txt_mv	Yang, Chen @@aut@@ Su, Hong-yong @@aut@@ An, Ning @@aut@@ Wu, Hong-luan @@aut@@ Guo, Xiao-yan @@aut@@ Li, Zhi-hang @@aut@@ Chen, Xiao-cui @@aut@@ Zhu, Shao-ping @@aut@@ Wu, Dan @@aut@@ Li, Hui-yuan @@aut@@ Pan, Qing-jun @@aut@@ Liang, Dong @@aut@@ Liu, Hua-feng @@aut@@
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author	Yang, Chen
spellingShingle	Yang, Chen misc Hyperuricemia misc Renal inflammation misc Renal fibrosis misc Urate deposition misc AMPK α2 AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model
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topic_title	AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model Hyperuricemia (dpeaa)DE-He213 Renal inflammation (dpeaa)DE-He213 Renal fibrosis (dpeaa)DE-He213 Urate deposition (dpeaa)DE-He213 AMPK α2 (dpeaa)DE-He213
topic	misc Hyperuricemia misc Renal inflammation misc Renal fibrosis misc Urate deposition misc AMPK α2
topic_unstemmed	misc Hyperuricemia misc Renal inflammation misc Renal fibrosis misc Urate deposition misc AMPK α2
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title	AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model
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title_full	AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model
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author_browse	Yang, Chen Su, Hong-yong An, Ning Wu, Hong-luan Guo, Xiao-yan Li, Zhi-hang Chen, Xiao-cui Zhu, Shao-ping Wu, Dan Li, Hui-yuan Pan, Qing-jun Liang, Dong Liu, Hua-feng
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title_sort	amp-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model
title_auth	AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model
abstract	Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney. © The Author(s) 2022
abstractGer	Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney. © The Author(s) 2022
abstract_unstemmed	Abstract Hyperuricemia can induce acute and chronic kidney damage, but the pathological mechanism remains unclear. The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. In summary, AMPK α2 is involved in acute and chronic hyperuricemia-induced kidney injury and may be associated with increased urate crystal deposition in the kidney. © The Author(s) 2022
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title_short	AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model
url	https://dx.doi.org/10.1186/s40001-022-00800-1
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author2	Su, Hong-yong An, Ning Wu, Hong-luan Guo, Xiao-yan Li, Zhi-hang Chen, Xiao-cui Zhu, Shao-ping Wu, Dan Li, Hui-yuan Pan, Qing-jun Liang, Dong Liu, Hua-feng
author2Str	Su, Hong-yong An, Ning Wu, Hong-luan Guo, Xiao-yan Li, Zhi-hang Chen, Xiao-cui Zhu, Shao-ping Wu, Dan Li, Hui-yuan Pan, Qing-jun Liang, Dong Liu, Hua-feng
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The potential role of AMP-activated protein kinase (AMPK) α2 in hyperuricemia-induced renal injury was investigated in this study. Acute and chronic hyperuricemic nephropathy was induced by administering intraperitoneal injections of uric acid and oxonic acid to AMPK α2 knockout and wild-type mice. Changes in renal function, histopathology, inflammatory cell infiltration, renal interstitial fibrosis, and urate deposition were analyzed. In both acute and chronic hyperuricemic nephropathy mouse models, knockout of AMPK α2 significantly reduced serum creatinine levels and renal pathological changes. The tubular expression of kidney injury molecule-1 was also reduced in hyperuricemic nephropathy mice deficient in AMPK α2. In addition, knockout of AMPK α2 significantly suppressed the infiltration of renal macrophages and progression of renal interstitial fibrosis in mice with chronic hyperuricemic nephropathy. Knockout of AMPK α2 reduced renal urate crystal deposition, probably through increasing the expression of the uric acid transporter, multidrug resistance protein 4. 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AMP-activated protein kinase α2 contributes to acute and chronic hyperuricemic nephropathy via renal urate deposition in a mouse model

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