Circulating autophagy regulator Rubicon is linked to increased myocardial infarction risk

Bibliographic Details
Title: Circulating autophagy regulator Rubicon is linked to increased myocardial infarction risk
Authors: Marie-Hélène Grazide, Jean-Bernard Ruidavets, Wim Martinet, Meyer Elbaz, Cécile Vindis
Source: Journal of Molecular and Cellular Cardiology Plus, Vol 11, Iss , Pp 100279- (2025)
Publisher Information: Elsevier, 2025.
Publication Year: 2025
Collection: LCC:Diseases of the circulatory (Cardiovascular) system
Subject Terms: Rubicon, Autophagy, Biomarker, Myocardial infarction, Risk prediction, Diseases of the circulatory (Cardiovascular) system, RC666-701
More Details: Background: The identification of new biomarkers that improve existing cardiovascular risk prediction models for acute coronary syndrome is essential for accurately identifying high-risk patients and refining treatment strategies. Autophagy, a vital cellular degradation mechanism, is important for maintaining cardiac health. Dysregulation of autophagy has been described in cardiovascular conditions such as myocardial ischemia-reperfusion injury, a key factor in myocardial infarction (MI). Recently, Rubicon (Run domain Beclin-1-interacting and cysteine-rich domain-containing protein), a key negative regulator of autophagy, has been identified in the modulation of cardiac stress response. Objectives: This study aimed to explore the relationship between circulating Rubicon levels and MI, and to evaluate the incremental predictive value of Rubicon when integrated into a clinical risk prediction model for MI. Results: We analyzed plasma Rubicon concentrations in 177 participants, comprising type I MI patients and high-risk control subjects. Our results revealed significantly elevated plasma Rubicon levels in MI patients compared to the control group (126.5 pg/mL vs. 53 pg/mL, p
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2772-9761
Relation: http://www.sciencedirect.com/science/article/pii/S2772976124001326; https://doaj.org/toc/2772-9761
DOI: 10.1016/j.jmccpl.2024.100279
Access URL: https://doaj.org/article/2b01cb0e146e40718c8ceec04fdc4ee3
Accession Number: edsdoj.2b01cb0e146e40718c8ceec04fdc4ee3
Database: Directory of Open Access Journals
More Details
ISSN:27729761
DOI:10.1016/j.jmccpl.2024.100279
Published in:Journal of Molecular and Cellular Cardiology Plus
Language:English