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Updated: Jan 1, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Gal-3 (Galectin-3) and KCa3.1 Mediate Heterogeneous Cell Coupling and Myocardial Fibrogenesis Driven by βAR

Gang She1, Meng-Chen Hou1,2, Yu Zhang1

  • 1From the Department of Physiology and Pathophysiology (G.S., M.-C.H., Yu Zhang, Yi Zhang, Y.W., X.-J.D., X.-L.D.), Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.

Hypertension (Dallas, Tex. : 1979)
|December 17, 2019
PubMed

Keywords:
fibroblastfibrosisgalectin-3heart failureinflammationcardiac fibrosis mechanismsβ-adrenoceptor signalingfibroblast activation pathwaysTRPV4 channel function

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