ArticleCell death and differentiation2026
USP13 ameliorates diabetic cardiomyopathy via deubiquitinating NLRP3 and inhibiting pyroptosis in cardiomyocytes.
Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- MicroRNA-223-3p/NLRP3 axis attenuates LPS-induced sepsis-like myocardial dysfunction by suppressing cardiomyocyte pyroptosis.Molecular biology reports · 2026Article
- Cardiomyocyte-Derived USP20 Attenuates Diabetic Cardiomyopathy by Facilitating the Degradation of STING and Mitigating STING-Mediated Inflammation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- NLRP3-mediated pyroptosis in cardiovascular disease: from molecular mechanisms to therapeutic targets.Frontiers in pharmacology · 2026Review
- Inflammasomes as the molecular hub of cardiovascular-metabolic-immune comorbidity networks.Frontiers in immunology · 2025Review
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Authors and funding
10 authors.
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Abstract
Diabetic cardiomyopathy (DCM) is a leading cause of diabetes-related mortality. Identifying new functional proteins in DCM pathology and elucidating the underlying mechanisms may provide new therapeutic targets for this disease. Here, we observed that the expression of the deubiquitinating enzyme USP13 was significantly downregulated in DCM mouse heart tissues. We discovered that the expression of USP13 was predominantly localized in cardiomyocytes. Cardiomyocyte-specific knockout of USP13 exacerbated myocardial injury in both type I and type II diabetic mice. Conversely, overexpression of USP13 in cardiomyocytes via recombinant adeno-associated virus 9 (AAV9) showed therapeutic effects against DCM in mice. Interestingly, using co-precipitation and LC-MS/MS analysis, we identified the NOD-like receptor family pyrin domain containing 3 (NLRP3) as a target protein of USP13 in cardiomyocytes. Mechanistically, we have illustrated that USP13 removes the K63-linked ubiquitin chain at K557 of NLRP3 to inhibit NLRP3-ASC interaction, thereby inhibiting ASC polymerization and the activation of NLRP3 inflammasome complex, ultimately alleviating pyroptosis in HG + PA challenged cardiomyocytes. Importantly, we showed that the cardioprotective effects of USP13 overexpression depended on NLRP3, as evidenced by the loss of protection in NLRP3-deficient diabetic mice. Taken together, this study identifies the protective impact and molecular regulation of USP13 in DCM pathology, uncovering a novel cardiomyocyte-specific USP13-NLRP3 axis in DCM.
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