Academic Journal
Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.
| Τίτλος: | Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions. |
|---|---|
| Συγγραφείς: | Yi L; School of Pharmacy, Nantong University, 9 Seyuan Road, Nantong, Jiangsu, 226019, China., Chen T; School of Pharmacy, Nantong University, 9 Seyuan Road, Nantong, Jiangsu, 226019, China., Zhou Y; School of Pharmacy, Nantong University, 9 Seyuan Road, Nantong, Jiangsu, 226019, China., Zhu P; Xinglin College, Nantong University, 9 Seyuan Road, Nantong, Jiangsu, 226019, China., Zhu Q; School of Pharmacy, Nantong University, 9 Seyuan Road, Nantong, Jiangsu, 226019, China., Shao Y; School of Pharmacy, Nantong University, 9 Seyuan Road, Nantong, Jiangsu, 226019, China., Yao W; School of Pharmacy, Nantong University, 9 Seyuan Road, Nantong, Jiangsu, 226019, China. juanwenyy@ntu.edu.cn.; Department of Pharmacology, School of Pharmacy, Nantong University, 9 Seyuan Road, Nantong, Jiangsu, 226019, China. juanwenyy@ntu.edu.cn. |
| Πηγή: | Molecular biomedicine [Mol Biomed] 2026 May 25; Vol. 7 (1). Date of Electronic Publication: 2026 May 25. |
| Τύπος έκδοσης: | Journal Article; Review |
| Γλώσσα: | English |
| Στοιχεία περιοδικού: | Publisher: Springer Singapore Country of Publication: Singapore NLM ID: 9918283581406676 Publication Model: Electronic Cited Medium: Internet ISSN: 2662-8651 (Electronic) Linking ISSN: 26628651 NLM ISO Abbreviation: Mol Biomed Subsets: MEDLINE |
| Imprint Name(s): | Original Publication: Singapore : Springer Singapore, [2020]- |
| Ιατρικοί όροι (MeSH): | Neointima*/pathology , Neointima*/metabolism , Neointima*/therapy , Neointima*/genetics , Coronary Restenosis*/pathology , Coronary Restenosis*/metabolism , Coronary Restenosis*/therapy , Hyperplasia*, Muscle, Smooth, Vascular/metabolism ; Muscle, Smooth, Vascular/pathology ; MicroRNAs/genetics ; Humans ; Animals ; Signal Transduction |
| Περίληψη: | Vascular restenosis, a pathological recurrence of lumen narrowing following interventions, remains a major limitation to the long-term success of vascular procedures. Its development is centrally driven by neointimal hyperplasia, a process orchestrated by endothelial injury, phenotypic switching of vascular smooth muscle cells (VSMCs) from a contractile to a synthetic state, and a coordinated inflammatory response. Despite advancements, the molecular mechanisms are not fully elucidated, and specific, effective pharmacotherapies are still lacking. This review systematically delineates the pathophysiology, focusing on these three core elements, and provides a comprehensive landscape of the complex signaling networks and molecular targets. We extensively cover protein-based regulators-including pro-proliferative factors (e.g., LSD1, FGF10), protective mediators (e.g., CGRP, A20), dual-action molecules with isoform-specific or context-dependent effects (e.g., KLFs, HDACs), endothelial repair targets (e.g., VEGF), and molecules that coordinately target both VSMCs and endothelial cells (ECs) (e.g., PERK, METTL3). We place significant focus on non-coding RNAs, particularly microRNAs (miRNAs) like miR-221/222, which fine-tune multiple targets in both VSMCs and ECs, offering unique precision. We critically evaluate the therapeutic significance and clinical translation potential, while addressing formidable challenges: functional duality within protein families (e.g., KLFs, HDACs), difficulties in cell-specific delivery and stability for miRNA therapies, and a narrow therapeutic window. Additionally, we highlight the emerging role of the vascular adventitia as a key source of regulatory signals (e.g., FGF10). By integrating insights from molecular mechanisms to therapeutic interventions, this work serves as a valuable reference for identifying novel strategies to combat neointima formation and vascular restenosis. (© 2026. The Author(s).) |
| Competing Interests: | Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare that they have no competing interests. |
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| Grant Information: | JC2023041 National Natures Science Foundation of Nantong City; KYCX25_3838 Postgraduate Research & Practice Innovation Program of Jiangsu Province; 81970226 National Natural Sciences Foundation of China |
| Contributed Indexing: | Keywords: Molecular targets; Neointimal hyperplasia; Phenotypic transformation; Re-endothelialization; Vascular restenosis |
| Substance Nomenclature: | 0 (MicroRNAs) |
| Entry Date(s): | Date Created: 20260524 Date Completed: 20260717 Latest Revision: 20260813 |
| Update Code: | 20260813 |
| PubMed Central ID: | PMC13199572 |
| DOI: | 10.1186/s43556-026-00477-6 |
| PMID: | 42178457 |
| Βάση Δεδομένων: | MEDLINE |
| ISSN: | 2662-8651 |
|---|---|
| DOI: | 10.1186/s43556-026-00477-6 |