ArticleJournal of the American Heart Association2026
Stanniocalcin-1 Attenuates Cardiac Fibrosis Post Ischemia-Reperfusion Injury by Targeting the DOCKER Domain of Dedicator of Cytokinesis 1.
Article in Journal of the American Heart Association, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundCardiac fibrosis is a pivotal pathological process driving heart failure following ischemia-reperfusion (I/R) injury. STC1 (stanniocalcin-1), a conserved glycoprotein with mitochondrial regulatory functions, remains unexplored in myocardial fibrosis. This study investigates the mechanistic role of cardiomyocyte-derived STC1 in cardiac fibrosis.
methodsMouse models of myocardial I/R injury were established by left anterior descending coronary artery ligation followed by 24-hour reperfusion. Cardiac-specific STC1 knockdown (adeno-associated virus 9-shSTC1) or overexpression (adeno-associated virus 9-STC1) preceded I/R injury induction. Cardiac function was assessed via echocardiography, and fibrosis was quantified histologically (Masson's trichrome, Sirius red) and molecularly (α-SMA [alpha smooth muscle actin], COL1A1 [collagen type I alpha 1 chain], COL3A1 [collagen type III alpha 1 chain], Smad2 [SMAD family member 2]). In vitro, cardiomyocyte-derived conditioned medium was applied to TGF-β (transforming growth factor beta)-stimulated fibroblasts, supplemented with recombinant STC1 for rescue assays. Protein-protein interactions were analyzed via coimmunoprecipitation and domain-deletion mutants.
resultsSTC1 deficiency exacerbated post-I/R cardiac dysfunction and fibrosis, accompanied by elevated α-SMA, COL1A1, and phosphorylated-Smad2 levels. Conversely, STC1 overexpression attenuated I/R-induced functional decline and fibrosis. In addition, cardiomyocyte-derived STC1 suppressed TGF-β-driven fibroblast activation and Smad2 nuclear translocation. Mechanistically, STC1 directly interacted with the DOCKER domain of DOCK1 (dedicator of cytokinesis 1), disrupting DOCK1/RAC1-GTP (Rac family small GTPase 1 bound to guanosine triphosphate) signaling. Genetic ablation of the DOCKER domain abolished STC1's antifibrotic effects, restoring RAC1-GTP activity and fibrosis markers.
conclusionsCardiomyocyte-derived STC1 mitigates cardiac fibrosis post I/R by targeting the DOCK1/RAC1 axis via its interaction with the DOCKER domain. These findings identify STC1-DOCK1 as a novel therapeutic pathway for ischemic heart failure.
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