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Study breakdown

VIP Receptor Genetic Variants Linked to Rheumatoid Arthritis

Clinical TrialModerate evidence
The takeaway

Genetic polymorphisms in the VIP receptor (VPAC1) were associated with rheumatoid arthritis, with RA patients showing altered VIP signaling — genetic evidence for the neuropeptide anti-inflammatory pathway in autoimmunity.

Key finding

VPAC1 receptor gene polymorphisms were associated with RA susceptibility, with RA patients showing altered VIP receptor expression and signaling — pro

What the researchers found

VPAC1 receptor gene polymorphisms were associated with RA susceptibility, with RA patients showing altered VIP receptor expression and signaling — providing genetic evidence linking the neuropeptide anti-inflammatory system to autoimmune disease pathogenesis.

Why it matters

Relevant for neuropeptides, inflammation, immune-function.

How the study worked

clinical-trial study.

What this study cannot tell us

See abstract.

How to read the evidence

moderate evidence.

When this study was published

Published in 2008.

The bigger picture

Advances peptide research.

Questions still open

  • Further research needed.
  • Clinical translation to evaluate.

Common questions

What was studied?
VIP Receptor Genetic Variants Linked to Rheumatoid Arthritis
What was found?
Genetic polymorphisms in the VIP receptor (VPAC1) were associated with rheumatoid arthritis, with RA patients showing altered VIP signaling — genetic evidence for the neuropeptide anti-inflammatory pathway in autoimmunity.

Read the original research

Genetic association of vasoactive intestinal peptide receptor with rheumatoid arthritis: altered expression and signal in immune cells.

Arthritis and rheumatism, 58(4), 1010-9

Citation

Delgado, Mario; Robledo, Gema; Rueda, Blanca; Varela, Nieves; O'Valle, Francisco; Hernandez-Cortes, Pedro; Caro, Marta; Orozco, Gisela; Gonzalez-Rey, Elena; Martin, Javier. (2008). Genetic association of vasoactive intestinal peptide receptor with rheumatoid arthritis: altered expression and signal in immune cells.. Arthritis and rheumatism, 58(4), 1010-9. https://doi.org/10.1002/art.23482