Title : Metformin protects high glucose‑cultured cardiomyocytes from oxidative stress by promoting NDUFA13 expression and mitochondrial biogenesis via the AMPK signaling pathway.

Pub. Date : 2020 Dec

PMID : 33174032






9 Functional Relationships(s)
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1 Metformin protects high glucose-cultured cardiomyocytes from oxidative stress by promoting NDUFA13 expression and mitochondrial biogenesis via the AMPK signaling pathway. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
2 Metformin, an AMP-activated protein kinase (AMPK) activator, protects cardiomyocytes from oxidative stress by improving mitochondrial function; however, the exact underlying mechanisms are not completely understood. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
3 Metformin, an AMP-activated protein kinase (AMPK) activator, protects cardiomyocytes from oxidative stress by improving mitochondrial function; however, the exact underlying mechanisms are not completely understood. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
4 Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
5 Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
6 Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
7 Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
8 Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus
9 Moreover, metformin promoted mitochondrial NDUFA13 protein expression via the AMPK signaling pathway, which was abolished by pretreatment with the AMPK inhibitor, Compound C. The results suggested that metformin protected cardiomyocytes against HG-induced oxidative stress via a mechanism involving AMPK, NDUFA13 and mitochondrial biogenesis. Metformin protein kinase AMP-activated catalytic subunit alpha 2 Rattus norvegicus