Inhibition of galectin-3 post-infarction impedes progressive fibrosis by regulating inflammatory profibrotic cascades.

ABSTRACT:

Aims

Acute myocardial infarction (MI) causes inflammation, collagen deposition, and reparative fibrosis in response to myocyte death and, subsequently, a pathological myocardial remodelling process characterized by excessive interstitial fibrosis, driving heart failure (HF). Nonetheless, how or when to limit excessive fibrosis for therapeutic purposes remains uncertain. Galectin-3, a major mediator of organ fibrosis, promotes cardiac fibrosis and remodelling. We performed a preclinical assessment of a protein inhibitor of galectin-3 (its C-terminal domain, Gal-3C) to limit excessive fibrosis resulting from MI and prevent ventricular enlargement and HF.

Methods and results

Gal-3C was produced by enzymatic cleavage of full-length galectin-3 or by direct expression of the trunc

SUBMITTER: Wang X 

PROVIDER: S-EPMC10676456 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature