LMCD1 peggiora la fibrosi cardiaca dopo infarto miocardico attivando STAT5A.

Cardiac fibrosis, a maladaptive remodeling process following myocardial infarction (MI), is a key driver of heart failure, the precise molecular regulators governing cardiac fibroblast activation remain incompletely understood. LIM and cysteine-rich domains 1 (LMCD1) has been shown to promote renal and lung fibrosis, but its role in cardiac fibrosis is unknown. We hypothesized that LMCD1 promoted cardiac fibrosis post-MI. Re-analysis of publicly available single-cell RNA sequencing datasets revealed a significant upregulation of LMCD1 in cardiac fibroblasts after MI. LMCD1 was upregulated in mouse hearts subjected to left anterior descending (LAD) artery ligation and in primary cardiac fibro