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 |