Autophagy regulates cellular senescence by mediating the degradation of CDKN1A/p21 and CDKN2A/p16 through SQSTM1/p62-mediated selective autophagy in myxomatous mitral valve degeneration.

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Tác giả: Brendan M Corcoran, Vicky E MacRae, Greg R Markby, Maciej Parys, Kanchan Phadwal, Keyi Tang, Qiyu Tang

Ngôn ngữ: eng

Ký hiệu phân loại: 343.0122 Military, defense, public property, public finance, tax, commerce (trade), industrial law

Thông tin xuất bản: United States : Autophagy , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 644357

Myxomatous mitral valve degeneration (MMVD) is one of the most important age-dependent degenerative heart valve disorders in both humans and dogs. It is characterized by the aberrant remodeling of extracellular matrix (ECM), regulated by senescent myofibroblasts (aVICs) transitioning from quiescent valve interstitial cells (qVICs), primarily under TGFB1/TGF-β1 control. In the present study, we found senescent aVICs exhibited impaired macroautophagy/autophagy as evidenced by compromised autophagy flux and immature autophagosomes. MTOR-dependent autophagy induced by rapamycin and torin-1 attenuated cell senescence and decreased the expression of cyclin-dependent kinase inhibitors (CDKIs) CDKN2A/p16
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