Fibroblasts‐specific p16INK4a exacerbates inflammageing‐mediated post‐infarction ventricular remodelling through interacting with STAT3 to regulate NLRP3 transcription

Fibroblasts‐specific p16INK4a exacerbates inflammageing‐mediated post‐infarction ventricular remodelling through interacting with STAT3 to regulate NLRP3 transcription

Abstract Background and Aims Inflammageing represents both a critical pathophysiological hallmark and independent risk factor for myocardial infarction (MI), with age‐related increases observed in MI incidence and severity of post‐MI ventricular remodelling. Novel therapeutic strategies targeting in...

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Main Authors: Xin Gu, Yingqiang Du, Jin'ge Zhang, Jiyu Li, Haiyun Chen, Yujie Lin, Yue Wang, Chunli Zhang, Shiyu Lin, Nannan Hao, Chengyi Peng, Jiacheng Ge, Jin Liu, Yan Liang, Yongjie Zhang, Xiaoyan Wang, Fang Wang, Jianliang Jin
Format: Article
Language:English
Published: Wiley 2025-06-01
Series:Clinical and Translational Medicine
Subjects:
nanotherapy
NLRP3 inflammasome
p16INK4a
post‐infarction ventricular remodelling
STAT3
Online Access:https://doi.org/10.1002/ctm2.70344
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https://doi.org/10.1002/ctm2.70344

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