ArticleJournal of cellular and molecular medicine2024
Regulation of Clusterin in the Heart and Plasma of Mice After Transverse Aortic Constriction.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Isovolumic relaxation strain imaging is an accurate and sensitive approach for detection of active diastolic dysfunction: A preclinical study.Animal models and experimental medicine · 2026Article
- Clusterin activates the heat shock response via the PI3K/Akt pathway to protect cardiomyocytes from high-temperature-induced apoptosis.Open life sciences · 2025Article
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Authors and funding
11 authors.
Funding
Abstract
Chronic pressure overload induces adverse cardiac remodelling characterised by left ventricular (LV) hypertrophy and fibrosis, leading to heart failure (HF). Identification of new biomarkers for adverse cardiac remodelling enables us to better understand this process and, consequently, to prevent HF. We recently identified clusterin (CLU) as a biomarker of cardiac remodelling and HF after myocardial infarction. The aim of this study was to investigate whether CLU expression is regulated in the heart and could be used as an indicator of adverse cardiac remodelling in response to pressure overload. We quantified CLU in the LV of mice subjected to transverse aortic constriction (TAC) and observed increased CLU mRNA levels and its mature protein form (m-CLU) compared to the sham. Interestingly, CLU mRNA levels were positively correlated with pro-hypertrophic (ANP, BNP, B-MHC), pro- and anti-fibrotic (TGFb, ColI and CILP) genes. In addition, m-CLU was positively correlated with LV hypertrophy, LV end diastolic and systolic diameters, and negatively correlated with LV ejection fraction. Finally, we observed that m-CLU levels only increased in TAC mice with severe cardiac remodelling and dysfunction without any significant difference in plasma CLU levels. This is the first study to demonstrate that cardiac expression of CLU is induced in the LV of TAC mice during adverse cardiac remodelling. However, plasma CLU levels could not be used as biomarkers of TAC-induced cardiac remodelling and dysfunction.
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Registered trials
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