Novel association of NAV3 with dilated cardiomyopathy and its role in cardiac fibrosis

American Journal of Physiology-Heart and Circulatory Physiology 2026

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Authors: Min wang, Rachad Ghazal, Akshatha N. Srinivas, Thanh Thanh L. Nguyen, Vishakantha Murthy, D. McNamara, Michelle Skime, Anthony Batzler, Gregory D. Jenkins, Simona Barlera, Silvana Pileggi, Luisa Mestroni
+9 more Marco Merlo, Florence Pinet, Jan Krejčí, Anna Chaloupka, Pascal. De Groote, RM Weinshilboum, Daniel J. Tschumperlin, Duan Liu, Naveen Pereira
DOI: 10.1152/ajpheart.00806.2025
Cited by: 2
References: 63

Abstract

This study uncovers a previously unrecognized role for NAV3 in TGF-β1-driven cardiac fibroblast activation. We show that NAV3 facilitates profibrotic remodeling through noncanonical signaling and cell cycle arrest, independently of SMAD2/3. These findings position NAV3 as a novel regulator of fibroblast phenotype and a potential modulator of cardiac fibrosis.

Fields of Study & Subjects

Cardiac Fibrosis and Remodeling Congenital heart defects research Cardiomyopathy and Myosin Studies

Publication details

Journal / source
American Journal of Physiology-Heart and Circulatory Physiology
Publisher
American Physiological Society
Volume
330
Issue
3
Pages
H686–H696
Publication date
29 January 2026
Language
EN