ReviewCurrent atherosclerosis reports2025
Statins as Modulators of Epithelial to Mesenchymal Transition in Cardiovascular-Kidney-Metabolic Syndrome: a Comprehensive Review of Mechanisms and Therapeutic Implications.
Review in Current atherosclerosis reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed.
- Cardiovascular-kidney-metabolic syndrome: a comprehensive review of pathophysiology, epidemiology, diagnosis, and management.Cardiovascular diabetology · 2026Review
- Emerging multidimensional biomarker system for cardiovascular-kidney-metabolic syndrome: from multi-omics integration to clinical artificial intelligence.Cardiovascular diabetology · 2026Review
- Life-Course Regulation of Health and Disease by Nitric Oxide: Mechanistic Insights.Antioxidants (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewCardiovascular-kidney-metabolic (CKM) syndrome involves complex interactions among cardiovascular, renal, and metabolic disorders. This review provides an overview of the mechanistic aspects of the epithelial-mesenchymal transition (EMT) and analyzes the regulatory impact of various statins on EMT-associated signaling pathways. RECENT
findingsEMT and endothelial-to-mesenchymal transition (EndoMT) are crucial in the development of cardiac fibrosis, vascular remodeling, and interstitial fibrosis. Several signaling pathways, including the TGF-β/Smad, Wnt/β-catenin, MAPK, and Notch signaling pathways, as well as oxidative stress and inflammatory mediators, regulate these processes. Statins exert significant biological effects by downregulating proinflammatory cytokines, suppressing ROS, and inhibiting EMT-related signaling pathways. Statins can also inhibit EndoMT and reduce the progression of vascular fibrosis and atherosclerosis in the context of cardiovascular diseases. Similarly, in renal disorders such as chronic kidney disease (CKD) and diabetic nephropathy, statins reduce EMT in renal tubular epithelial cells by targeting pathways such as Smad and MAPK. CKM syndrome involves complex interactions among cardiovascular, renal, and metabolic disorders. Among the factors implicated in the pathophysiology of CKM, the EMT process is recognized as a key biological process. Evidence from preclinical and clinical studies supports the emerging role of statins as promising agents in managing CKM through modulating EMT. Therefore, understanding the diverse mechanisms of statins may lead to the development of more effective therapeutic strategies against CKM's fibrotic and inflammatory complications.
Indexed as
Identifiers
41231308What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.