CYLD exaggerates pressure overload-induced cardiomyopathy via suppressing autolysosome efflux in cardiomyocytes

Deubiquitinating enzymes (DUBs) appear to be a new class of regulators of cardiac homeostasis and disease. However, DUB-mediated signaling in the heart is not well understood. Herein we report a novel mechanism by which cylindromatosis (CYLD), a DUB mediates cardiac pathological remodeling and dysfunction. Cardiomyocyte-restricted (CR) overexpression of CYLD (CR-CYLD) did not cause gross health issues and hardly affected cardiac function up to age of one year in both female and male mice at physiological conditions.

Source: Journal of Molecular and Cellular Cardiology - June 13, 2020 Category: Cytology Authors: Lei Qi, Huimei Zang, Weiwei Wu, Prakash Nagarkatti, Mitzi Nagarkatti, Qinghang Liu, Jeffrey Robbins, Xuejun Wang, Taixing Cui Source Type: research