ArticleCardiovascular diabetology2026
Myeloid Cdc42 deficiency-mediated macrophage pyroptosis exacerbates diabetic cardiomyopathy in type 1 diabetes mellitus.
Article in Cardiovascular diabetology, 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
backgroundDiabetic cardiomyopathy (DCM) is one of the severe complications in type 1 diabetes mellitus (T1DM) patients with impaired cardiac function and faster progression to heart failure due to systolic malfunction. It has been demonstrated that macrophage-mediated chronic inflammation is closely associated with DCM. Cell division cycle 42 (Cdc42) plays a crucial role in regulating the polarization, migration and phagocytosis of macrophages, however, the underlying mechanism of Cdc42 in DCM remains to be elucidated.
methodsMouse DCM models with T1DM were generated using myeloid-specific Cdc42-knockout (Cdc42
resultsMyeloid Cdc42 deletion exacerbated T1DM-induced cardiac dysfunctions and histopathological changes including cardiac fibrosis, and promoted T1DM-induced macrophage infiltration and M1 polarization of macrophages, and facilitated T1DM-induced pyroptosis by activating NLRP3 inflammasome in the hearts in mice. Notably, there were no significant differences between Cdc42
conclusionsThis study demonstrates that myeloid Cdc42 deficiency or inhibition aggravates T1DM-induced cardiomyocyte injury and cardiac fibrosis of DCM by promoting macrophage pyroptosis and inflammatory responses, which might provide a novel therapeutic target for immunomodulatory intervention in DCM of type 1 diabetes mellitus.
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