The DOI matches its Crossref record; 81 of the 81 references it cites were found in a registry or an index.
ICAM-1 and VCAM-1: Gatekeepers in various inflammatory and cardiovascular disorders
Abstract
Leukocyte migration from the vascular compartment is critical fornormal lymphocyte recirculation in specific tissues and immune response in inflammatory locations. Leukocyte recruitment, migration to inflammatory areas, and targeting in the extravascular space are caused by cellular stimulation and local expression of adhesion molecules. Intercellular adhesion molecule 1 (ICAM-1) and Vascular cell adhesion molecule 1 (VCAM-1) belong to the immunoglobulin superfamily of cell adhesion molecules with a crucial role in mediating the strong adherence of leukocytes to endothelial cells in numerous acute as well as chronic diseases. ICAM-1 and VCAM-1 mediate inflammation and promote leukocyte migration during inflammation. ICAM-1 and VCAM-1 have a large role in regulating homeostasis and in pathologic statessuch as cancer, atherosclerosis, atrial fibrillation, myocardial infarction, stroke, asthma, obesity, kidney diseases, and much more. In inflammatory conditions and infectious disorders, leukocytes move and cling to the endothelium via multiple intracellular adhesive interactions. It is suggested that combining membrane-bound and soluble ICAM-1 and VCAM-1 into a single unit functional system will further our understanding of their immunoregulatory role as well as their pathophysiologic effects in disease. This review focuses on the pathophysiologic roles of ICAM-1 and VCAM-1 in various inflammatory and other diseases as well as their emerging cardiovascular role during the COVID-19 pandemic.
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Cites
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ICAM-1 signaling in endothelial cells
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Cited by
Cell-cell communication: New insights and clinical implications
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Endothelial Dysfunction as the Common Pathway Linking Obesity, Hypertension and Atherosclerosis
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Metadata
- Authors
- Singh, V., Kaur, R., Kumari, P., Pasricha, C., & Singh, R.
- Venue
- Clinica Chimica Acta
- Publisher
- Elsevier BV
- Published
- 2023-08
- Volume
- 548
- Pages
- 117487
- ISSN
- 0009-8981 (ISSN-L)
- OpenAlex
- W4383879255
- Cited by
- 432
- References
- 81
- FWCI
- 65.66
- Type
- journal article
- Language
- en
- Open access
- closed
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