UCP2 overexpression activates SIRT3 to regulate oxidative stress and mitochondrial dynamics induced by myocardial injury

Geng, Zhengguang; Chen, Wenbo; Lu, Qinju; Fu, Bao; Fu, Xiaoyun

doi:10.1016/j.abb.2024.109918

Archives of Biochemistry and Biophysics

2024

DOI: 10.1016/j.abb.2024.109918

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UCP2 overexpression activates SIRT3 to regulate oxidative stress and mitochondrial dynamics induced by myocardial injury

Zhengguang Geng,

Wenbo Chen,

Qinju Lu

et al.

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2024

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Cited by 4 publications

References 33 publications

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Fenofibrate reduces cardiac remodeling by mitochondrial dynamics preservation in a renovascular model of cardiac hypertrophy

Castiglioni,

Gelosa,

Muluhie

et al. 2024

European Journal of Pharmacology

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Fenofibrate reduces cardiac remodeling by mitochondrial dynamics preservation in a renovascular model of cardiac hypertrophy

Castiglioni,

Gelosa,

Muluhie

et al. 2024

European Journal of Pharmacology

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Epigenetic regulation of diverse regulated cell death modalities in cardiovascular disease: Insights into necroptosis, pyroptosis, ferroptosis, and cuproptosis

Chen,

Wang,

Zhang

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Redox Biology

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Mitochondrial uncoupling protein 2: a central player in pancreatic disease pathophysiology

Wang,

Zhang,

Deng

et al. 2024

Mol Med

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Pancreatic diseases pose considerable health challenges due to their complex etiology and limited therapeutic options. Mitochondrial uncoupling protein 2 (UCP2), highly expressed in pancreatic tissue, participates in numerous physiological processes and signaling pathways, indicating its potential relevance in these diseases. Despite this, UCP2’s role in acute pancreatitis (AP) remains underexplored, and its functions in chronic pancreatitis (CP) and pancreatic steatosis are largely unknown. Additionally, the mechanisms connecting various pancreatic diseases are intricate and not yet fully elucidated. Given UCP2’s diverse functionality, broad expression in pancreatic tissue, and the distinct pathophysiological features of pancreatic diseases, this review offers a comprehensive analysis of current findings on UCP2’s involvement in these conditions. We discuss recent insights into UCP2’s complex regulatory mechanisms, propose that UCP2 may serve as a central regulatory factor in pancreatic disease progression, and hypothesize that UCP2 dysfunction could significantly contribute to disease pathogenesis. Understanding UCP2’s role and mechanisms in pancreatic diseases may pave the way for innovative therapeutic and diagnostic approaches. Graphical Abstracts

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UCP2 overexpression activates SIRT3 to regulate oxidative stress and mitochondrial dynamics induced by myocardial injury

Cited by 4 publications

References 33 publications

Fenofibrate reduces cardiac remodeling by mitochondrial dynamics preservation in a renovascular model of cardiac hypertrophy

Fenofibrate reduces cardiac remodeling by mitochondrial dynamics preservation in a renovascular model of cardiac hypertrophy

Epigenetic regulation of diverse regulated cell death modalities in cardiovascular disease: Insights into necroptosis, pyroptosis, ferroptosis, and cuproptosis

Mitochondrial uncoupling protein 2: a central player in pancreatic disease pathophysiology

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