Activated Protein C Suppresses Cardiomyocyte Senescence in Diabetic Cardiomyopathy via PAR1/PAR3-P85-CaMKIIδ Axis.

Yueqi Zhang, Lei Dai, Mengwen Wang, Xiaodan Zhong, Xiaolei Liu, Kaiyue Zhang, Lingyun Luo, Lingyun Wang, Wei Dong, Alexandra Vaczy, Lina Li, Tamas Atlasz, Thati Madhusudhan, Chang Xu, Hongjie Wang, Hesong Zeng

Department of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. · pubmed

Paper

Abstract

Diabetes exacerbates cardiomyocyte senescence, leading to an accelerated decline in cardiac function. The systemic levels of activated protein C (aPC) were reduced, which correlated with deterioration of cardiac diastolic function in diabetic cardiomyopathy (DbCM), while the underlying mechanisms remained unclear. We aim to identify the role of aPC in ameliorating cardiomyocyte senescence in DbCM. We highlighted that aPC ameliorated cardiomyocyte senescence in DbCM via the PAR1/PAR3-P85-CaMKIIδ axis with genetic (TMP/P) and interventional (PC injection) diabetic mouse models. These findings could lead to increased insight into the pathogenesis and innovative therapeutic approaches of diabetic cardiomyopathy.

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Research summary

Activated protein C ameliorates cardiomyocyte senescence in diabetic cardiomyopathy via the PAR1/PAR3-P85-CaMKIIδ axis. The study addresses a mechanism related to cellular senescence in the context of diabetes, which is a significant factor in aging and age-related diseases, thus contributing to the understanding of longevity.

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