β 2 -Adrenergic receptor disruption exacerbates cardiac injury and fibroblast activation in a female mouse model of Takotsubo cardiomyopathy

American Journal of Physiology-Cell Physiology 2026 Open access

Read full text
Authors: Bruno Sanches, Fernanda Tupini, Fernando Espanhol, Pedro Augusto Carvalho Costa, Gabriel Matos Nogueira, Iago Pinheiro, Fernando Souza-Neto, Alexander Birbrair, Pedro Pires Goulart Guimarães, Marina Gomes Miranda e Castor, Jop H. van Berlo, Sílvia Guatimosim
DOI: 10.1152/ajpcell.00087.2026
Cited by: 1
References: 31

Abstract

Takotsubo cardiomyopathy (TTC) disproportionately affects women and is driven by excessive β-adrenergic receptor (βAR) activation. We show that loss of β 2 AR signaling exacerbates myocardial injury, creating a proinflammatory and profibrotic milieu that amplifies fibroblast activation and reshapes their paracrine profile. These activated cardiac fibroblasts (CFs) further sustain cardiomyocyte hypertrophy, perpetuating the injury loop in β 2 AR-deficient hearts. These findings establish β 2 AR as a determinant of cardiac resilience and support β 2 AR-directed strategies as interventions in the acute phase of TTC.

Fields of Study & Subjects

Takotsubo Cardiomyopathy and Associated Phenomena Cardiac Fibrosis and Remodeling Pericarditis and Cardiac Tamponade

Publication details

Journal / source
American Journal of Physiology-Cell Physiology
Publisher
American Physiological Society
Volume
331
Issue
3
Pages
C747–C758
Publication date
16 June 2026
Language
EN