ArticleAmerican journal of physiology. Cell physiology2026
Retinoic acid promotes expression of inflammatory factors in proliferative adult human heart cells.
Article in American journal of physiology. Cell physiology, 2026. 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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Who cites it
2 citing papers in PubMed.
- Increased Retinol Levels in Patients with Cardiac Surgery-Associated Acute Kidney Injury-A Prospective Single-Center Exploratory Study.Nutrients · 2026Article
- Metabolic, viral, and immune phenotypes in long COVID.Frontiers in endocrinology · 2026Article
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Authors and funding
5 authors.
Funding
Abstract
Retinoid signaling is increased in the hearts of patients with coronary artery disease and during acute myocardial infarction (MI). The effects of retinoids on cardiac repair after injury remain incompletely understood. Our laboratory has derived proliferative cardiac cell clones from adult human left ventricle biopsies and is investigating how these cells might participate in cardiac repair in heart failure. We treated clones isolated from unique individuals with retinoic acid (RA) and performed unbiased proteomics, bioinformatic analyses, and targeted follow-up experiments to identify and confirm RA-regulated factors and processes. RA increased the expression of well-known proinflammatory proteins including interleukin-1 (IL1A and B) and inducible cyclooxygenase 2 (COX2), while decreasing the expression of extracellular matrix (ECM) factors such as thrombospondin 1 and collagens. Additionally, we found that basal expression of retinoid metabolizing enzymes (e.g., ALDH1A3) significantly correlated with expression of cytokines and inflammatory mediators including IL1A/B and COX2 across clones from different donors. Secretion of IL1B by clones was found to respond to physiological and pharmacological doses of RA, and monocyte migration in vitro responded to secretions from RA-treated clones. Our findings suggest a mechanism by which retinoids promote inflammation and contribute to adverse cardiac remodeling in the injured heart, providing a potential avenue to regulate myocardial inflammation and remodeling processes.
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