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Study summary · research use only

Role of vasoactive intestinal peptide in osteoarthritis

Review · human · Journal of biomedical science · 2016 · DOI 10.1186/s12929-016-0280-1 · PMID 27553659

Plain-language summary

Paraphrased from the published abstract below — not a verdict on whether anything works.

This review article (species: human, based on studies of osteoarthritis patients) discusses vasoactive intestinal peptide (VIP) and its reported roles in cardiac contractility, vasodilation, neuroendocrine-immune communication, blood pressure regulation, and anti-inflammatory/immune-modulatory activity. It states VIP has been reported to prevent chronic cartilage damage and joint remodeling in osteoarthritis (OA), and that VIP is down-regulated in OA synovial fluid, which the authors associate with increased pro-inflammatory cytokine production potentially contributing to OA pathogenesis; it also notes contradictory reports that VIP accumulation in joints may contribute to OA. The review describes studies indicating up-regulation of VIP can counteract pro-inflammatory stimuli and reduce pain in OA, and calls for further clinical investigation.

Abstract

Vasoactive intestinal peptide (VIP) plays important roles in many biological functions, such as, stimulation of contractility in the heart, vasodilation, promoting neuroendocrine-immune communication, lowering arterial blood pressure, and anti-inflammatory and immune-modulatory activity. Osteoarthritis (OA) is a chronic and degenerative bone disease, which is one of the most common causes of disability and most common in both sexes as people become older. Interestingly VIP can prevent chronic cartilage damage and joint remodeling. This review article provides update information on the association of VIP and OA and its treatment. Evidences suggest that VIP is down-regulated in synovial fluid of OA, and VIP down-regulation leads to increase in the production of pro-inflammatory cytokines that might contribute to the pathogenesis of OA; however contradictory reports also exist suggesting that accumulation of VIP in joints can also contribute OA. A number of studies indicated that up-regulation of VIP can counteract the action of pro-inflammatory stimuli and alleviate the pain in OA. More clinical investigations are necessary to determine the biology of VIP and its therapeutic potential in OA that might represent the future standards of care for OA.

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