New research data on the causes of white finger syndrome
The FinnGen research project has produced new information on the causes of white fingering, or Raynaud’s disease. The study found eight genes that affect the immune system and blood circulation. In particular, the adrenergic signal system proved important in the development of Raynaud’s disease, especially in cold conditions.
An international study led by the University of Helsinki identified several genetic risk factors for Raynaud’s disease and demonstrated for the first time their biological mechanism of action at the cellular level. The results were published in the scientific journal Cell Genomics. The study showed that genes associated with the risk of Raynaud’s disease are related to the susceptibility of blood vessels to contraction and the body’s defense mechanisms. Some of the identified risk genes affect how blood vessels respond to neurotransmitters such as adrenaline and nitric oxide.
The study was carried out by utilising Finnish FinnGen research material and other extensive genetic research data. The findings obtained by studying genes were verified by laboratory tests in small blood vessel cells in collaboration with Stanford University. The study highlighted biological mechanisms in Raynaud’s disease both in cellular models and at the population level, and clarified the role of immune defense and circulatory regulation in disease risk and cell function.
Raynaud’s disease is caused by exceptionally strong narrowing of small blood vessels, for example when the fingers are exposed to cold. The fingers first turn white, bluish at the end of blood flow, and finally turn reddish as blood returns to the small blood vessels. This phenomenon occurs in about 3-5% of the population. Typically, the phenomenon is not accompanied by other symptoms, but sometimes it is caused by some other disease.
In particular, the study confirmed the association of the adrenergic signal system with Raynaud’s disease. Certain forms of the ADRA2A gene were found to increase the risk of disease. In cell experiments, it was found that a receptor encoded by the ADRA2A gene affects the contractility of smooth muscle cells in small blood vessels in a cold environment. This study showed that the disease is transmitted through a receptor encoded by the ADRA2A gene, whereas previous research has focused on the ADRA2C gene.