Key result
TRIM proteins regulate cardiovascular homeostasis, inflammation, and remodeling via context-dependent ubiquitination.
Why the study?
Current cardiovascular therapies mostly target downstream pathological manifestations rather than upstream regulatory mechanisms governing stress adaptation and tissue remodeling. Emerging evidence implicates tripartite motif proteins as context-dependent regulators across a wide spectrum of cardiovascular diseases.
This review delineates the biochemical features and cell-specific mechanistic roles of TRIM family E3 ubiquitin ligases in cardiovascular pathogenesis, highlighting their potential and challenges as diagnostic biomarkers and therapeutic targets.
Answers are grounded in this paper and cite their sources.
TRIM proteins merit targeted investigation as upstream regulators in cardiovascular disease; leaves open their validation as biomarkers or therapies in prospective studies.
Cardiovascular diseases are driven by sustained mechanical stress, metabolic derangement, inflammation and oxidative injury, which progressively disrupt cellular homeostasis within the heart and vasculature.Although current therapeutic strategies have substantially improved clinical outcomes, most interventions primarily target downstream pathological manifestations rather than upstream regulatory mechanisms that determine stress adaptation and tissue remodeling.Tripartite motif (TRIM) proteins constitute a large family of E3 ubiquitin ligases characterized by a highly conserved RBCC domain architecture and diversified C-terminal regions.By catalyzing distinct ubiquitin chain topologies and functioning as molecular scaffolds, TRIM proteins broadly regulate protein turnover, inflammatory signaling, metabolic adaptation and cell fate determination.Emerging evidence identifies TRIM proteins as context-dependent regulators whose biological effects are shaped by cell type, disease stage and microenvironmental conditions.Multiple TRIM family members have been linked to a wide spectrum of cardiovascular diseases, including atherosclerosis, vascular calcification, myocardial infarction, cardiac hypertrophy and metabolic cardiomyopathy.At the cellular level, TRIM proteins influence disease initiation and progression by modulating endothelial dysfunction, vascular smooth muscle cell phenotypic remodeling, cardiomyocyte survival and metabolic homeostasis, fibroblast activation and immune-inflammatory responses.The present review summarized the biochemical characteristics and cell-specific functions of TRIM proteins and delineates their mechanistic roles in cardiovascular pathogenesis.In addition, it discussed their emerging potential as diagnostic biomarkers and therapeutic targets, highlighting both translational opportunities and context-dependent challenges.Contents 1. Introduction 2. Structural features and classification of TRIM proteins 3. Roles of TRIM proteins in cardiovascular cell types 4. Roles of TRIM proteins in vascular diseases 5. Roles of TRIM proteins in cardiac diseases 6. TRIM proteins as biomarkers and therapeutic targets 7. Conclusions and future perspectives
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Wang et al. (2026) conducted a review in Cardiovascular diseases (including atherosclerosis, vascular calcification, myocardial infarction, cardiac hypertrophy, and metabolic cardiomyopathy). Tripartite motif (TRIM) proteins was evaluated. TRIM proteins act as context-dependent E3 ubiquitin ligases and molecular scaffolds regulating cellular homeostasis, inflammation, and remodeling across cardiovascular diseases.
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