@article {10.3844/ojbsci.2026.26.03.052,
article_type = {journal},
title = {Adipokines Overview: The Major Component of Immune Dysregulation},
author = {Poznyak, Anastasia Vladimirovna and Borodko, Daria Dmitryevna and Antonov, Stanislav Anatolievich and Rozhkova, Ulyana Vyacheslavovna and Pavshintsev, Vsevolod Vyacheslavovich and Orekhov, Alexander Nikolaevich},
volume = {26},
number = {3},
year = {2026},
month = {Aug},
pages = {52-1},
doi = {10.3844/ojbsci.2026.26.03.052},
url = {https://thescipub.com/abstract/ojbsci.2026.26.03.052},
abstract = {Purpose of Review: Obesity is increasingly recognized as an immune endocrine disorder rather than only a metabolic condition. This review critically examines how adipokines particularly adiponectin, resistin, adipsin, and chemerin mediate the interplay between obesity and autoimmunity. Unlike previous reviews that broadly surveyed cytokines, our focus is on comparative roles of specific adipokines across multiple autoimmune diseases. Recent Findings: Evidence demonstrates that these adipokines exert dual and sometimes contradictory immunomodulatory effects, shaping both metabolic dysfunction and autoimmune activity. Elevated adiponectin, resistin, and adipsin are observed in systemic lupus erythematosus and rheumatoid arthritis, while chemerin strongly correlates with psoriasis and multiple sclerosis activity. However, the clinical interpretation is complicated by differential effects of adipokine isoforms and context-specific receptor signaling. Summary: A critical gap remains in distinguishing protective versus pathogenic adipokine actions and in understanding how adipose-derived versus tissue-localized adipokines differentially influence disease progression. Future research should standardize measurement of adipokine isoforms, explore causal pathways through longitudinal and mechanistic studies, and evaluate whether targeting adipokines could provide dual benefits in obesity-related and autoimmune disorders.},
journal = {OnLine Journal of Biological Sciences},
publisher = {Science Publications}
}