Research published in Aging Cell identifies Gas6, a protein secreted by senescent cells, as a driver of aortic valve calcification. The signal activates a CaMKII–DRP1 pathway that governs the terminal scission of mitochondrial-derived vesicles, linking cellular senescence and mitochondrial quality control to the stiffening of cardiac valve tissue. Calcific aortic valve disease is a leading age-related cardiovascular condition with no approved pharmacological treatment.
Key Points
- Gas6 from senescent cells promotes aortic valve calcification.
- CaMKII–DRP1 signaling controls mitochondrial-derived vesicle terminal scission.
- Mitochondrial quality control links senescence to valve stiffening.
Longevity Analysis
Valve calcification has long been treated as passive mineral deposition; framing it as an actively signaled process places it within reach of intervention. The implicated chain runs from accumulated senescent cells through secreted signaling factors to mitochondrial waste handling inside valve cells, meaning the integrity of energy production and cellular housekeeping directly shapes how well blood moves through an aging heart. Reducing senescent cell burden and supporting mitochondrial turnover become structural cardiovascular strategies, not merely metabolic ones.
Original published by Wiley Aging Cell, by Yaoyu Zhang, Jialiang Zhang, Yanjiani Xu, Wenhua Lei, Fei Xu, Junli Li, Zisong Wei, Bo Su, Shuang Liu, Jing Zhou, Hongde Li, Junpeng Ran, Weiya Li, Tuerhongjiang Tuerdi, Xiaojiao Wang, Zhi Fang, Fangyang Huang, Mao Chen .