Molecular and cellular basis of the pathogenesis of vibration disease (narrative literature review)

Vibration disease occupies a leading place in the structure of occupational pathology in the Russian Federation. Its progressive course leads to incapacity for work and disability in individuals of employable age. This necessitates the identification of early markers of damage, which is impossible without a detailed understanding of the sequence of pathological changes that precede the appearance of clinical and functional manifestations of the disease.

The aim of the study. Generalization and analysis of contemporary data on the molecular and cellular basis of the pathogenesis of vibration disease.

The following databases were used to search and select literature sources: eLIBRARY, PubMed, Google Scholar, MedLine, Web of Science, and Scopus. The vibration disease is a systemic pathological process based on a cascade of interconnected molecular and cellular disturbances. Vibration exposure is accompanied by the development of oxidative stress, combined with mitochondrial dysfunction and disruption of bioenergetic processes, creates conditions for damage to cellular structures. The central link in the pathogenesis is endothelial dysfunction, developing from reversible vasomotor disturbances to persistent vascular wall remodeling. It is based on damage to the ultrastructure of endothelial cells, an imbalance of vasoactive molecules, and the activation of proinflammatory and proapoptotic signaling pathways. Activation of the sympathoadrenal system and the renin-angiotensin-aldosterone system further contributes to the aggravation of vasoconstriction and trophic disturbances. Endothelial changes and associated tissue hypoxia trigger immune system involvement, manifested by cytokine profile imbalances, changes in lymphocyte subpopulation composition, and suppression of innate immunity. There the relationship of the formed disorders with damage to the nervous tissue, confirmed by an increase in neurospecific proteins and the development of secondary autoimmune responce.

Conclusion. The performed analysis allows expanding our understanding of the pathogenetic basis of vibration disease for the elaboration of up-to-date strategies for early diagnosis, prevention, and treatment of the disease.

Contribution:
Bugaeva M.S. – concept and design of the study, collection and analysis of literature data, writing the text, editing;
Gostyaeva E.P. – collection and analysis of literature data, writing the text;
Zhukova A.G. – collection and analysis of literature data;
Gorokhova L.G. – collection and analysis of literature data;
Bondarev O.I. – collection and analysis of literature data.
All authors are responsible for the integrity of all parts of the manuscript and approval of the manuscript final version.

Conflict of interest. The authors declare no conflict of interest.

Funding. The study had no sponsorship.

Received: April 24, 2026 / Revised: May 25, 2026 / Accepted: July 1, 2026 / Published: August 14, 2026

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