ArticleFrontiers in physiology2026
MiR-199a family members are differentially regulated during physiological and pathological cardiac hypertrophy.
Article in Frontiers in physiology, 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
Among potential molecular mechanisms supporting cardiovascular homeostasis, miRNAs (miRs) represent interesting candidates. We recently highlighted that miR-199a controls the Nitric oxide synthase/nitric oxide (NOS/NO) pathway in the endothelium and showed that both mature strands of miR-199a are overexpressed in heart and vessels from a mouse model of hypertension. Here we investigated the fate of miR-199a in heart and vessels from mice developing physiological or pathological cardiac hypertrophy. Our working hypothesis is that alterations in cell phenotypes driven by changes in miR-199a abundance account for cardiac and/or vascular adaptation to increased workload in patho-physiological contexts. C57BL/6J mice were given access to voluntary dynamic wheel training during 22 weeks or underwent transverse aortic constriction (TAC) surgery. As a result, those mice respectively developed physiological and pathological cardiac hypertrophy. An opposite modulation of miR-199a-3p and miR-199a-5p expression was observed in vessels and heart from running
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