ArticleFrontiers in pharmacology2025
Clusterin protects against HFpEF by inhibiting UCHL1-mediated NLRP3 deubiquitylation and inflammasome activation.
Article in Frontiers in pharmacology, 2025. 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
Background: Heart failure with preserved ejection fraction (HFpEF) poses a serious threat to human health, but effective treatment strategies remain limited. Clusterin (CLU) is a multifunctional glycoprotein implicated in inflammation and tissue remodeling, but its role in HFpEF pathogenesis is not fully understood. Methods: The effects of CLU in a murine HFpEF model were investigated by adeno-associated virus (AAV)-mediated overexpression and liver-specific knockout approaches. Cardiac function in mice was evaluated by echocardiography, and myocardial inflammation and fibrosis were assessed using Masson's trichrome staining, real-time qPCR, and Western blot analysis. Protein interactions were identified by immunoprecipitation-mass spectrometry (IP-MS). Results: AAV-mediated CLU overexpression significantly improved diastolic function and reduced myocardial inflammation and fibrosis in HFpEF mice, whereas liver-specific CLU knockout aggravated disease progression. Conclusion: This study reveals a novel regulatory mechanism through which CLU alleviates HFpEF by modulating the UCHL1-NLRP3 signaling axis. The findings provide new insight into the anti-inflammatory and anti-fibrotic roles of CLU and suggest that CLU and its derived peptide hold translational potential as therapeutic candidates for HFpEF.
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