Stelios Psarras and his colleagues recently published a study in Cellular and Molecular Life Sciences Journal

In this work Stelios Psarras and colleagues use a genetic model of cardiomyopathy and progressive heart failure to establish a detrimental role for galectin-3 in heart failure and associated comorbidities and to support its targeting in intervention strategies. They reveal previously unidentified mechanisms of galectin-3 action; loss-of-function of galectin-3 is shown to constrain cardiac dysfunction and adverse remodeling including fibrosis by altering the macrophage-fibroblast cross talk and by facilitating repair activities exerted by cardiac fibroblasts during an early inflammatory stage. Moreover, galectin-3 loss-of-function is also shown to protect from an emphysema-like pulmonary defect, a heart failure comorbid condition.

Pubmed

Galectin-3 interferes with tissue repair and promotes cardiac dysfunction and comorbidities in a genetic heart failure model.
Vlachou F, Varela A, Stathopoulou K, Ntatsoulis K, Synolaki E, Pratsinis H, Kletsas D, Sideras P, Davos CH, Capetanaki Y, Psarras S. Cell Mol Life Sci. 2022 Apr 19;79(5):250. doi: 10.1007/s00018-022-04266-6.