Communications biology · 2024
PEX3 promotes regenerative repair after myocardial injury in mice through facilitating plasma membrane localization of ITGB3.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Sun Jia-Teng, Wang Zi-Mu, Zhou Liu-Hua, Yang Tong-Tong, Zhao Di, Bao Yu-Lin, Wang Si-Bo, Gu Ling-Feng, Chen Jia-Wen, Shan Tian-Kai, Wei Tian-Wen, Wang Hao, Wang Qi-Ming, Kong Xiang-Qing, Xie Li-Ping, Gu Ai-Hua, Zhao Yang, Chen Feng, Ji Yong, Cui Yi-Qiang, Wang Lian-Sheng
Аннотация
The peroxisome is a versatile organelle that performs diverse metabolic functions. PEX3, a critical regulator of the peroxisome, participates in various biological processes associated with the peroxisome. Whether PEX3 is involved in peroxisome-related redox homeostasis and myocardial regenerative repair remains elusive. We investigate that cardiomyocyte-specific PEX3 knockout (Pex3-KO) results in an imbalance of redox homeostasis and disrupts the endogenous proliferation/development at different times and spatial locations. Using Pex3-KO mice and myocardium-targeted intervention approaches, the effects of PEX3 on myocardial regenerative repair during both physiological and pathological stages are explored. Mechanistically, lipid metabolomics reveals that PEX3 promotes myocardial regenerative repair by affecting plasmalogen metabolism. Further, we find that PEX3-regulated plasmalogen activates the AKT/GSK3β signaling pathway via the plasma membrane localization of ITGB3. Our study indicates that PEX3 may represent a novel therapeutic target for myocardial regenerative repair following injury.