Mitochondrial outer membrane protein Samm50 protects against hypoxia-induced cardiac injury by interacting with Shmt2

Zhou, Yufei; Kang, Le; Xu, Ran; Zhao, Di; Wang, Jienan; Wu, Jiaying; Lin, Hong; Ding, Zhiwen; Zou, Yunzeng

doi:10.1016/j.cellsig.2024.111219

Cellular Signalling

2024

DOI: 10.1016/j.cellsig.2024.111219

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Mitochondrial outer membrane protein Samm50 protects against hypoxia-induced cardiac injury by interacting with Shmt2

Yufei Zhou,

Le Kang,

Ran Xu

et al.

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2024

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Cited by 2 publications

References 34 publications

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ORP5 promotes cardiac hypertrophy by regulating the activation of mTORC1 on lysosome

Zhao,

Xu,

Zhou

et al. 2024

Journal of Advanced Research

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ORP5 promotes cardiac hypertrophy by regulating the activation of mTORC1 on lysosome

Zhao,

Xu,

Zhou

et al. 2024

Journal of Advanced Research

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ASK-1 activation exacerbates kidney dysfunction via increment of glomerular permeability and accelerates cellular aging in diabetic kidney disease model mice

Kajimoto,

Nagasu,

Takasu

et al. 2024

Sci Rep

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Diabetic kidney disease (DKD) is a major disease characterized by early albuminuria and heightened risk of renal deterioration. Increased reactive oxygen species (ROS) production, especially in glomeruli, plays an important role in the progression of DKD. ROS also cause activation of Apoptosis signal-regulating kinase 1 (ASK-1), which is implicated in various organ injuries. However, the detailed mechanisms remain unclear. This study investigates ASK-1 activation in advanced DKD and its underlying mechanisms using GS442172, an ASK-1 inhibitor. In the DKD mouse model, activation of ASK-1 was observed. Although inhibition of ASK-1 activation improved hyperpermeability in glomerular endothelial cells. ASK-1 inhibition significantly reduced glomerular injury and albuminuria, while also attenuating tubular damage and interstitial fibrosis. RNA-seq analysis revealed an aging phenotype associated with ASK-1 activation in DKD. In vitro experiments demonstrated ASK-1 activation-induced cellular senescence in tubular cells via redox signaling. These results suggested that the critical role of ASK-1 activation in DKD pathogenesis, implicating glomerular injury, tubular damage, and cellular senescence. ASK-1 inhibitors are promising therapeutic strategies to mitigate the progression of DKD.

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Mitochondrial outer membrane protein Samm50 protects against hypoxia-induced cardiac injury by interacting with Shmt2

Cited by 2 publications

References 34 publications

ORP5 promotes cardiac hypertrophy by regulating the activation of mTORC1 on lysosome

ORP5 promotes cardiac hypertrophy by regulating the activation of mTORC1 on lysosome

ASK-1 activation exacerbates kidney dysfunction via increment of glomerular permeability and accelerates cellular aging in diabetic kidney disease model mice

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