Key result
Fibroblast primary cilia deletion reduces post-MI fibrosis and improves LVEF in mice.
Why the study?
Does the deletion of primary cilia on cardiac fibroblasts reduce cardiac fibrosis and improve cardiac function after myocardial infarction in mice?
Does the deletion of primary cilia on cardiac fibroblasts reduce cardiac fibrosis and improve cardiac function after myocardial infarction in mice?
Ablation of primary cilia on cardiac fibroblasts attenuates fibrosis and preserves cardiac output after myocardial infarction by downregulating Hedgehog signaling, presenting a novel cellular mechanism and therapeutic target.
Positions fibroblast cilia as a novel antifibrotic target; leaves open translation to human post-MI therapy.
Cardiomyocytes die and do not regenerate after an injury such as a myocardial infarction (MI), a leading cause of mortality worldwide. Following MI, cardiac fibroblasts (CFs) proliferate and differentiate into myofibroblasts, which then produce increased collagen and extracellular matrix (ECM) leading to fibrosis. Fibrosis can weaken cardiac output via excessive stiffening and interference with electric signal transmission, but can also prevent wall rupture under load (reviewed in (1)). Thus, dampening fibrosis has been investigated as a potential therapeutic intervention. Most mammalian cells possess a single primary cilium involved in intercellular communication. We investigated the role of CF primary cilia in sensing injury signals and initiating fibrotic remodeling. We found that deleting CF cilia reduced fibrosis and improved cardiac output after MI, demonstrating that cilia act as a signaling hub that amplifies the fibrotic response in the injured heart.
No takes yet. Share an insight, caveat, or question.
Liu et al. (2026) studied Myocardial Infarction. Targeted deletion of primary cilia in cardiac fibroblasts (Ift88 deletion) vs. Control littermates (lacking Cre allele or heterozygous for floxed allele) was evaluated on Collagen deposition (fibrosis) and cardiac function (ejection fraction and fractional shortening) post-myocardial infarction. Deleting primary cilia in cardiac fibroblasts significantly reduced cardiac fibrosis and improved ejection fraction and fractional shortening following myocardial infarction in mice.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: