Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (786 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The active alterations of vascular wall structures, often leading to elevated vascular resistance. It is associated with aging; atherosclerosis; diabetes mellitus; hypertension; pregnancy; pulmonary hypertension; and stroke, but is also a normal part of embryogenesis.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Remodelings, Vascular; Remodeling, Vascular; Vascular Remodelings; Pulmonary Arterial Remodeling; Arterial Remodeling, Pulmonary; Arterial Remodelings, Pulmonary; Pulmonary Arterial Remodelings; Remodeling, Pulmonary Arterial.
Where it fits in the MeSH classification
- Broader topics
- Pathological Conditions, Anatomical; Pathologic Processes; Angiogenesis; Cardiovascular Physiological Phenomena
- See also
- Neovascularization, Pathologic; Neovascularization, Physiologic
Related concepts
- Vascular Resistance
- Aging
- Atherosclerosis
- Diabetes Mellitus
- Hypertension
- Pregnancy
- Pulmonary Hypertension
- Stroke
- Embryogenesis
Research landscape
PubMed indexes 5,027 records tagged with the MeSH heading “Vascular Remodeling” (counts retrieved 2026-10-29). 2,661 of them (52.9%) were published from 2020 onward, and the busiest period so far is 2020 onward with 2,661 records.
Reviews account for 856 records (17.0%) and meta-analyses for 18. Randomized controlled trials number 30 (0.6%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 0 |
| 2000-2009 | 0 |
| 2010-2019 | 2,437 |
| 2020 onward | 2,661 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 856 | 17.0% |
| Meta-analyses | 18 | 0.4% |
| Randomized controlled trials | 30 | 0.6% |
Method: PubMed query "Vascular Remodeling"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.
Reading the evidence in cardiovascular medicine
Cardiovascular medicine has an unusually large body of randomized trials, so the type of outcome matters: hard clinical events such as death, heart attack and stroke carry more weight than changes in blood pressure, cholesterol or imaging markers that only predict risk. Observational studies can show associations but are confounded by age, lifestyle and other illness. Check whether a result is about prevention or treatment, the baseline risk of participants, and the absolute rather than only the relative size of any benefit.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
Single-cell transcriptomics reveals skewed cellular communication and phenotypic shift in pulmonary artery remodeling [1]
Abstract reading summary — source excerpts
- Opening excerpt
- A central feature of progressive vascular remodeling is altered smooth muscle cell (SMC) homeostasis; however, the understanding of how different cell populations contribute to this process is limited.
- Closing excerpt
- The current study provides a blueprint of cellular and molecular changes on a single-cell level that are defining the pathological vascular remodeling process.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (181 words)
A central feature of progressive vascular remodeling is altered smooth muscle cell (SMC) homeostasis; however, the understanding of how different cell populations contribute to this process is limited. Here, we utilized single-cell RNA sequencing to provide insight into cellular composition changes within isolated pulmonary arteries (PAs) from pulmonary arterial hypertension and donor lungs. Our results revealed that remodeling skewed the balanced communication network between immune and structural cells, in particular SMCs. Comparative analysis with murine PAs showed that human PAs harbored heterogeneous SMC populations with an abundant intermediary cluster displaying a gradient transition between SMCs and adventitial fibroblasts. Transcriptionally distinct SMC populations were enriched in specific biological processes and could be differentiated into 4 major clusters: oxygen sensing (enriched in pericytes), contractile, synthetic, and fibroblast-like. End-stage remodeling was associated with phenotypic shift of preexisting SMC populations and accumulation of synthetic SMCs in neointima. Distinctly regulated genes in clusters built nonredundant regulatory hubs encompassing stress response and differentiation regulators. The current study provides a blueprint of cellular and molecular changes on a single-cell level that are defining the pathological vascular remodeling process.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36099047 · DOI · PMC9714792
Treg cells promote decidual vascular remodeling and modulate uterine NK cells in pregnant mice [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Regulatory T (Treg) cells are essential for maternal immune tolerance of the fetus and placenta.
- Closing excerpt
- The findings provide insight into mechanisms linking impaired adaptive immune tolerance and altered spiral artery remodeling, 2 hallmark features of preeclampsia.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (199 words)
Regulatory T (Treg) cells are essential for maternal immune tolerance of the fetus and placenta. In preeclampsia, aberrant Treg cell tolerance is implicated, but how Treg cells affect the uterine vascular dysfunction thought to precede placental impairment and maternal vasculopathy is unclear. We used Foxp3-diphtheria toxin receptor mice to test the hypothesis that Treg cells are essential regulators of decidual spiral artery adaptation to pregnancy. Transient Treg cell depletion during early placental morphogenesis caused impaired remodeling of decidual spiral arteries, altered uterine artery function, and fewer Dolichos biflorus agglutinin+ uterine natural killer (uNK) cells, resulting in late-gestation fetal loss and fetal growth restriction. Replacing the Treg cells by transfer from wild-type donors mitigated the impact on uNK cells, vascular remodeling, and fetal loss. RNA sequencing of decidua revealed genes associated with NK cell function and placental extravillous trophoblasts were dysregulated after Treg cell depletion and normalized by Treg cell replacement. These data implicate Treg cells as essential upstream drivers of uterine vascular adaptation to pregnancy, through a mechanism likely involving phenotypic regulation of uNK cells and trophoblast invasion. The findings provide insight into mechanisms linking impaired adaptive immune tolerance and altered spiral artery remodeling, 2 hallmark features of preeclampsia.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 39656539 · DOI · PMC11790030
Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Pulmonary hypertension (PH) is a serious cardiovascular disease caused by a variety of pathogenic factors, which is characterized by increased pulmonary vascular resistance (PVR) and progressive elevation of mean pulmonary artery pressure (mPAP).
- Closing excerpt
- In this review, comprehensive academic databases such as PubMed, Embase, Web of Science, and Google Scholar were systematically searched to discuss studies relevant to human and animal PH, with a focus on vascular remodeling in PH.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (242 words)
Pulmonary hypertension (PH) is a serious cardiovascular disease caused by a variety of pathogenic factors, which is characterized by increased pulmonary vascular resistance (PVR) and progressive elevation of mean pulmonary artery pressure (mPAP). This disease can lead to right ventricular hypertrophy and, in severe cases, right heart failure and even death. Vascular remodeling-a pathological modification involving aberrant vasoconstriction, cell proliferation, apoptosis resistance, and inflammation in the pulmonary vascular system-is a significant pathological hallmark of PH and a critical process in its progression. Recent studies have found that vascular remodeling involves the participation of a diversity of cellular pathological alterations, such as the dysfunction of pulmonary artery endothelial cells (PAECs), the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs), the phenotypic differentiation of pulmonary artery fibroblasts, the inflammatory response of immune cells, and pericyte proliferation. This review focuses on the mechanisms and the intercellular crosstalk of these cells in the PH process, emphasizing recent advances in knowledge regarding cellular signaling pathways, inflammatory responses, apoptosis, and proliferation. To develop better treatments, a list of possible therapeutic approaches meant to slow down certain biological functions is provided, with the aim of providing new insights into the treatment of PH by simplifying the intricacies of these complex connections. In this review, comprehensive academic databases such as PubMed, Embase, Web of Science, and Google Scholar were systematically searched to discuss studies relevant to human and animal PH, with a focus on vascular remodeling in PH.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40362501 · DOI · PMC12072204
A Minimally Invasive Framework Reveals Region-Specific Cerebrovascular Remodeling in Aging Using Intravital Functional Ultrasound Imaging and Ultrasound Localization Microscopy (fUS-ULM) [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Aging impairs cerebrovascular structure and function, contributing to cognitive decline and dementia.
- Closing excerpt
- This study establishes a powerful, non-invasive, and repeatable investigative tool for future preclinical studies aimed at evaluating the efficacy of therapeutic interventions targeting vascular contributions to cognitive impairment and neurodegeneration.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (164 words)
Aging impairs cerebrovascular structure and function, contributing to cognitive decline and dementia. Here, a novel, high-resolution, intravital imaging platform is presented that combines functional ultrasound (fUS) and ultrasound localization microscopy (ULM) through a chronically implanted, polymethylpentene (TPX) cranial window, a transparent implant that enables ultrasound imaging through the skull. This approach enables intravital, longitudinal, minimally invasive assessment of cerebrovascular structure and function across cortical and deep brain regions. Leveraging this platform, a new method is developed to estimate resting cerebral blood flow (CBF) by integrating microbubble (MB) velocity data from fUS with microvascular geometry derived from ULM. Notably, a significant age-related decline in the cortical arteriole-to-venule ratio (AVR) is discovered, introducing a novel biomarker of structural cerebrovascular remodeling. It is also validated that fUS can reliably assess neurovascular coupling (NVC) responses in aged mice. This study establishes a powerful, non-invasive, and repeatable investigative tool for future preclinical studies aimed at evaluating the efficacy of therapeutic interventions targeting vascular contributions to cognitive impairment and neurodegeneration.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40946188 · DOI · PMC12767048
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Pathology and pathobiology of pulmonary hypertension: state of the art and research perspectives [5]
- Research article Cardiac fibrosis in myocardial infarction-from repair and remodeling to regeneration [6]
- Research article The placenta: a multifaceted, transient organ [7]
- Research article Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease [8]
- Research article Reassessing the Mechanisms of Acute Coronary Syndromes [9]
- Research article Angiotensin II and vascular injury [10]
References
- Crnkovic S, Valzano F, Fließer E, Gindlhuber J, Thekkekara Puthenparampil H, Basil M, et al.. Single-cell transcriptomics reveals skewed cellular communication and phenotypic shift in pulmonary artery remodeling. . 2022. PMID 36099047 · DOI · PMC9714792
- Hosking SL, Moldenhauer LM, Tran HM, Chan HY, Groome HM, Lovell EA, et al.. Treg cells promote decidual vascular remodeling and modulate uterine NK cells in pregnant mice. . 2024. PMID 39656539 · DOI · PMC11790030
- Dai J, Chen H, Fang J, Wu S, Jia Z. Vascular Remodeling: The Multicellular Mechanisms of Pulmonary Hypertension. . 2025. PMID 40362501 · DOI · PMC12072204
- Negri S, Nyul-Toth A, Milan M, Troyano-Rodriguez E, Tavakol S, Ihuoma J, et al.. A Minimally Invasive Framework Reveals Region-Specific Cerebrovascular Remodeling in Aging Using Intravital Functional Ultrasound Imaging and Ultrasound Localization Microscopy (fUS-ULM). . 2026. PMID 40946188 · DOI · PMC12767048
- Humbert M, Guignabert C, Bonnet S, Dorfmüller P, Klinger JR, Nicolls MR, et al.. Pathology and pathobiology of pulmonary hypertension: state of the art and research perspectives. Eur Respir J. 2019. PMID 30545970 · DOI · PMC6351340
- Talman V, Ruskoaho H. Cardiac fibrosis in myocardial infarction-from repair and remodeling to regeneration. Cell Tissue Res. 2016. PMID 27324127 · DOI · PMC5010608
- Burton GJ, Fowden AL. The placenta: a multifaceted, transient organ. Philos Trans R Soc Lond B Biol Sci. 2015. PMID 25602070 · DOI · PMC4305167
- Wang X, Khalil RA. Matrix Metalloproteinases, Vascular Remodeling, and Vascular Disease. Adv Pharmacol. 2018. PMID 29310800 · DOI · PMC5765875
- Libby P, Pasterkamp G, Crea F, Jang IK. Reassessing the Mechanisms of Acute Coronary Syndromes. Circ Res. 2019. PMID 30605419 · DOI · PMC6447371
- Montezano AC, Nguyen Dinh Cat A, Rios FJ, Touyz RM. Angiotensin II and vascular injury. Curr Hypertens Rep. 2014. PMID 24760441 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-29.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.