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 (674 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
Cytokine-induced cell adhesion molecule present on activated endothelial cells, tissue macrophages, dendritic cells, bone marrow fibroblasts, myoblasts, and myotubes. It is important for the recruitment of leukocytes to sites of inflammation. (From Pigott and Power, The Adhesion Molecule FactsBook, 1993, p154)
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: Vascular Cell Adhesion Molecule 1; Inducible Cell Adhesion Molecule 110; INCAM-110; VCAM-1; CD106 Antigen; Antigen, CD106; Antigens, CD106; Vascular Cell Adhesion Molecule.
Where it fits in the MeSH classification
- Broader topics
- Cell Adhesion Molecules
Research landscape
PubMed indexes 9,842 records tagged with the MeSH heading “Vascular Cell Adhesion Molecule-1” (counts retrieved 2026-10-31). 1,129 of them (11.5%) were published from 2020 onward, and the busiest period so far is 2000-2009 with 3,676 records.
Reviews account for 359 records (3.6%) and meta-analyses for 38. Randomized controlled trials number 363 (3.7%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,966 |
| 2000-2009 | 3,676 |
| 2010-2019 | 3,071 |
| 2020 onward | 1,129 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 359 | 3.6% |
| Meta-analyses | 38 | 0.4% |
| Randomized controlled trials | 363 | 3.7% |
Method: PubMed query "Vascular Cell Adhesion Molecule-1"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in drugs and chemicals
Studies of a chemical or drug can answer very different questions: what it is and how it behaves in cells and animals, how the body handles it, and whether it changes outcomes in people. Laboratory and animal findings often do not carry over to patients, and observational studies of exposures are confounded by who uses a substance and why. Nothing on this page is a recommendation to use, avoid, start or stop any substance or medicine; talk to a qualified clinician or pharmacist about your own situation. Check the dose, the species, the comparison group and whether a patient-relevant outcome was measured.
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.
Emerging Roles of Vascular Cell Adhesion Molecule-1 (VCAM-1) in Immunological Disorders and Cancer [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Tumor necrosis factor alpha (TNFα) is a pro-inflammatory cytokine that triggers the expression of inflammatory molecules, including other cytokines and cell adhesion molecules.
- Closing excerpt
- This review covers the role and relevance of VCAM-1 in inflammation, and also highlights the emerging potential of VCAM-1 as a novel therapeutic target in immunological disorders and cancer.
- 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 (117 words)
Tumor necrosis factor alpha (TNFα) is a pro-inflammatory cytokine that triggers the expression of inflammatory molecules, including other cytokines and cell adhesion molecules. TNFα induces the expression of intercellular cell adhesion molecule-1 and vascular cell adhesion molecule-1 (VCAM-1). VCAM-1 was originally identified as a cell adhesion molecule that helps regulate inflammation-associated vascular adhesion and the transendothelial migration of leukocytes, such as macrophages and T cells. Recent evidence suggests that VCAM-1 is closely associated with the progression of various immunological disorders, including rheumatoid arthritis, asthma, transplant rejection, and cancer. This review covers the role and relevance of VCAM-1 in inflammation, and also highlights the emerging potential of VCAM-1 as a novel therapeutic target in immunological disorders and cancer.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 29614819 · DOI · PMC5979609
Targeting endothelial vascular cell adhesion molecule-1 in atherosclerosis: drug discovery and development of vascular cell adhesion molecule-1-directed novel therapeutics [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Vascular cell adhesion molecule-1 (VCAM-1) has been well established as a critical contributor to atherosclerosis and consequently as an attractive therapeutic target for anti-atherosclerotic drug candidates.
- Closing excerpt
- This has prompted the need for a comprehensive review that recounts the evolution of VCAM-1-directed pharmaceuticals and addresses the current challenges in novel anti-atherosclerotic drug development.
- 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 (191 words)
Vascular cell adhesion molecule-1 (VCAM-1) has been well established as a critical contributor to atherosclerosis and consequently as an attractive therapeutic target for anti-atherosclerotic drug candidates. Many publications have demonstrated that disrupting the VCAM-1 function blocks monocyte infiltration into the sub-endothelial space, which effectively prevents macrophage maturation and foam cell transformation necessary for atherosclerotic lesion formation. Currently, most VCAM-1-inhibiting drug candidates in pre-clinical and clinical testing do not directly target VCAM-1 itself but rather down-regulate its expression by inhibiting upstream cytokines and transcriptional regulators. However, the pleiotropic nature of these regulators within innate immunity means that optimizing dosage to a level that suppresses pathological activity while preserving normal physiological function is extremely challenging and oftentimes infeasible. In recent years, highly specific pharmacological strategies that selectively inhibit VCAM-1 function have emerged, particularly peptide- and antibody-based novel therapeutics. Studies in such VCAM-1-directed therapies so far remain scarce and are limited by the constraints of current experimental atherosclerosis models in accurately representing the complex pathophysiology of the disease. This has prompted the need for a comprehensive review that recounts the evolution of VCAM-1-directed pharmaceuticals and addresses the current challenges in novel anti-atherosclerotic drug development.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37595265 · DOI · PMC10597632
Adiponectin and leptin induce VCAM-1 expression in human and murine chondrocytes [3]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundOsteoarthritis (OA) and rheumatoid arthritis (RA), the most common rheumatic diseases, are characterized by irreversible degeneration of the joint tissues.
- Closing excerpt
- ConclusionsTaken together, our results suggest that leptin and adiponectin could perpetuate cartilage-degrading processes by inducing also factors responsible of leukocyte and monocyte infiltration at inflamed joints.
- 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 (208 words)
BackgroundOsteoarthritis (OA) and rheumatoid arthritis (RA), the most common rheumatic diseases, are characterized by irreversible degeneration of the joint tissues. There are several factors involved in the pathogenesis of these diseases including pro-inflammatory cytokines, adipokines and adhesion molecules.ObjectiveUp to now, the relationship between adipokines and adhesion molecules at cartilage level was not explored. Thus, the aim of this article was to study the effect of leptin and adiponectin on the expression of VCAM-1 in human and murine chondrocytes. For completeness, intracellular signal transduction pathway was also explored.MethodsVCAM-1 expression was assessed by quantitative RT-PCR and western blot analysis upon treatment with leptin, adiponectin and other pertinent reagents in cultured human primary chondrocytes. Signal transduction pathways have been explored by using specific pharmacological inhibitors in the adipokine-stimulated human primary chondrocytes and ATDC5 murine chondrocyte cell line.ResultsHerein, we demonstrate, for the first time, that leptin and adiponectin increase VCAM-1 expression in human and murine chondrocytes. In addition, both adipokines have additive effect with IL-1β. Finally, we demonstrate that several kinases, including JAK2, PI3K and AMPK are at a play in the intracellular signalling of VCAM-1 induction.ConclusionsTaken together, our results suggest that leptin and adiponectin could perpetuate cartilage-degrading processes by inducing also factors responsible of leukocyte and monocyte infiltration at inflamed joints.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 23285079 · DOI · PMC3526577
Telomere Shortening Drives Atrial Fibrillation Through VCAM-1 Mediated Atrial Electrical and Structural Remodeling [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Telomere shortening is a hallmark of aging and has been implicated in cardiovascular disease, but its mechanistic link to atrial fibrillation (AF) remains elusive.
- Closing excerpt
- These findings establish a telomere-VCAM-1 axis that drives atrial remodeling and arrhythmogenesis in aging, and position VCAM-1 as a candidate therapeutic target for age-related AF.
- 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 (158 words)
Telomere shortening is a hallmark of aging and has been implicated in cardiovascular disease, but its mechanistic link to atrial fibrillation (AF) remains elusive. Using a high-throughput, single-gene-calibrated dot blot assay, we developed to quantify leukocyte telomere length (LTL). In age-stratified analyses, shorter LTL was associated with AF predominantly in individuals younger than 70 years. In telomerase-deficient (TERT-/-) mice with telomere dysfunction, higher AF inducibility, atrial electrical conduction slowing, and atrial fibrosis were observed. Transcriptomic profiling revealed significant alterations in extracellular matrix and cell adhesion pathways in response to telomere dysfunction. Subsequent validation identified vascular cell adhesion molecule-1 (VCAM-1) as a potential mediator linking telomere shortening to AF-related atrial remodeling. Functional inhibition of VCAM-1 reversed electrophysiological abnormalities, attenuated atrial fibrosis, normalized ECM gene expression-including Col1α1, α-SMA, and CD168-and reduced AF susceptibility by 30%. These findings establish a telomere-VCAM-1 axis that drives atrial remodeling and arrhythmogenesis in aging, and position VCAM-1 as a candidate therapeutic target for age-related AF.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41685883 · DOI · PMC12903549
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 Vascular cell adhesion molecule-1 expression and signaling during disease: regulation by reactive oxygen species and antioxidants [5]
- Research article CD105 is important for angiogenesis: evidence and potential applications [6]
- Research article ICAM-1 and VCAM-1: Gatekeepers in various inflammatory and cardiovascular disorders [7]
- Research article Inhibition of LFA-1/ICAM-1 and VLA-4/VCAM-1 as a therapeutic approach to inflammation and autoimmune diseases [8]
- Research article Vascular cell adhesion molecule-1 (VCAM-1)--an increasing insight into its role in tumorigenicity and metastasis [9]
- Research article VCAM-1 as a predictor biomarker in cardiovascular disease [10]
References
- Kong DH, Kim YK, Kim MR, Jang JH, Lee S. Emerging Roles of Vascular Cell Adhesion Molecule-1 (VCAM-1) in Immunological Disorders and Cancer. . 2018. PMID 29614819 · DOI · PMC5979609
- Pickett JR, Wu Y, Zacchi LF, Ta HT. Targeting endothelial vascular cell adhesion molecule-1 in atherosclerosis: drug discovery and development of vascular cell adhesion molecule-1-directed novel therapeutics. . 2023. PMID 37595265 · DOI · PMC10597632
- Conde J, Scotece M, López V, Gómez R, Lago F, Pino J, et al.. Adiponectin and leptin induce VCAM-1 expression in human and murine chondrocytes. . 2012. PMID 23285079 · DOI · PMC3526577
- Wang Z, Zhao R, Wang Y, Zhang N, Yang Q, Zhou Z, et al.. Telomere Shortening Drives Atrial Fibrillation Through VCAM-1 Mediated Atrial Electrical and Structural Remodeling. . 2026. PMID 41685883 · DOI · PMC12903549
- Cook-Mills JM, Marchese ME, Abdala-Valencia H. Vascular cell adhesion molecule-1 expression and signaling during disease: regulation by reactive oxygen species and antioxidants. Antioxid Redox Signal. 2011. PMID 21050132 · DOI · PMC3151426
- Duff SE, Li C, Garland JM, Kumar S. CD105 is important for angiogenesis: evidence and potential applications. FASEB J. 2003. PMID 12773481 · DOI
- Singh V, Kaur R, Kumari P, Pasricha C, Singh R. ICAM-1 and VCAM-1: Gatekeepers in various inflammatory and cardiovascular disorders. Clin Chim Acta. 2023. PMID 37442359 · DOI
- Yusuf-Makagiansar H, Anderson ME, Yakovleva TV, Murray JS, Siahaan TJ. Inhibition of LFA-1/ICAM-1 and VLA-4/VCAM-1 as a therapeutic approach to inflammation and autoimmune diseases. Med Res Rev. 2002. PMID 11857637 · DOI
- Schlesinger M, Bendas G. Vascular cell adhesion molecule-1 (VCAM-1)--an increasing insight into its role in tumorigenicity and metastasis. Int J Cancer. 2015. PMID 24771582 · DOI
- Troncoso MF, Ortiz-Quintero J, Garrido-Moreno V, Sanhueza-Olivares F, Guerrero-Moncayo A, Chiong M, et al.. VCAM-1 as a predictor biomarker in cardiovascular disease. Biochim Biophys Acta Mol Basis Dis. 2021. PMID 34000374 · 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 2026-10-31.
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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.