Key result
Specific blockage of cardiac TRIF effectively decreased Ang-II/aldosterone-induced cardiac inflammation, fibrosis, hypertrophy, and dysfunction in mice.
Why the study?
Angiotensin II induces cardiac structural disorders and dysfunction, but the underlying molecular mechanisms are still not fully disclosed.
Does specific blockage of cardiac TRIF reduce Angiotensin-II-induced cardiac inflammation, fibrosis, hypertrophy, and dysfunction in mice?
Does specific blockage of cardiac TRIF reduce Angiotensin-II-induced cardiac inflammation, fibrosis, hypertrophy, and dysfunction in mice?
The TRIF/EGFR signalling axis mediates Angiotensin-II-induced cardiac remodelling, suggesting cardiac TRIF as a potential therapeutic target for heart failure and cardiac dysfunction.
Supports TRIF blockade in Ang-II remodeling models; hypothesis-generating and requires human validation before clinical consideration.
The excessive activation of renin-angiotensin system (RAS) is one of key pathophysiological characteristics in the development of cardiac remodelling. Angiotensin (Ang) II, as a main active peptide in RAS, induces cardiac structural disorders and dysfunction. However, the molecular mechanisms are still not fully disclosed. Present study aimed to determine the role and potential mechanisms of cardiac TIR-domain-containing adapter-inducing interferon-β (TRIF) in Ang-II-mediated cardiac remodelling in mice. In vitro and in vivo studies showed Ang II and downstream aldosterone obviously increased the expression of TRIF, accompanied with cardiac structural abnormalities and functional injuries. Specific blockage of cardiac TRIF effectively decreased Ang-II/aldosterone-induced cardiac inflammation, fibrosis, hypertrophy and dysfunction in mice. Mechanistically, the TRIF triggered the activation of EGF receptor (EGFR) signalling by nuclear factor (NF)-κB transcriptional regulation and downstream EGFR ligands. Taken together, present study supported that cardiac TRIF was a potential therapeutic target for attenuating cardiac pathophysiological remodelling. The TRIF/EGFR axis partially explained the molecular mechanism of Ang-II/aldosterone-induced cardiac inflammation, fibrosis, hypertrophy and dysfunction in mice.
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Zhu et al. (2020) studied Angiotensin-II-induced cardiac remodelling. Specific blockage of cardiac TRIF was evaluated on Cardiac inflammation, fibrosis, hypertrophy and dysfunction. Specific blockage of cardiac TRIF effectively decreased Ang-II/aldosterone-induced cardiac inflammation, fibrosis, hypertrophy, and dysfunction in mice.
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