Nature communications · 2026
PCSK5 promotes angiogenesis and cardiac repair after myocardial infarction.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Guo Jieyu, Ma Siyu, Ma Jinghua, Liu Ming, Ge Fei, Wang Xinhong, Lin Jiayi, Jiang Nan, Lin Xiaoke, Lian Zhipeng, Zuo Zheng, Li Liliang, Cao Genmao, Li Yongbo, Wei Xiangxiang, Ng Xianlong, Zhi Xiuling, Osto Elena, Dai Yuxiang, Li Jun, Wang Lixin, Jiang Hong, Meng Dan
Аннотация
PCSK5 (proprotein convertase subtilisin/kexin 5) is essential for heart development. However, its role in myocardial infarction (MI) remains unexplored. In this study, we found that the plasma levels of PCSK5 were elevated in MI patients and exhibited potential in predicting cardiac function improvement. PCSK5 expression was upregulated in cardiac endothelial cells (ECs) of MI patients. Pcsk5 deficiency in ECs impaired angiogenesis and cardiac recovery post-MI, and delayed tissue repair following hindlimb ischemic injury in male mice. In contrast, the endothelial-specific Pcsk5 delivery enhanced angiogenesis and cardiac function post-MI. Mechanistically, PCSK5 directly cleaved VEGFA, activating its signaling and promoting angiogenic activity. The residues Arg158 and Asn164 of PCSK5 were crucial for its function. Semaglutide increased vascular densities and cardiac function post-MI, partially through EC-derived Pcsk5 in male mice. This study identified PCSK5 as a pro-angiogenic factor secreted by ECs, with the potential to become a therapeutic target for ischemic diseases.