Absence of muscle atrophy in some rheumatic diseases: fundamental and applied aspects of paradoxical preservation of inflammatory muscles

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Abstract

Introduction. Although chronic inflammation is typically associated with tissue catabolism and wasting, most autoimmune rheumatic diseases, including polymyositis, dermatomyositis, lupus myositis, and overlap myopathies, as a rule paradoxically display preserved muscle trophism, despite significant weakness and pathohistological signs of inflammation. Only inclusion body myositis (IBM) typically exhibits progressive and irreversible muscle atrophy.

Aim. This article proposes the hypothesis that a unique immunometabolic equilibrium in rheumatic myopathies maintains muscle mass despite inflammation and provides a review of data supporting it.

Material and methods. PubMed/MEDLINE, EMBASE, elibrary.ru and Scielo bibliographic databases were screened for articles on “Rheumatic diseases” AND “Muscle preservation” as well as on “Muscle preservation” AND “Organokines” OR “Cytokines” between 1965 and 2025, without any language restrictions.

We discuss possible mechanisms involving mitochondrial biogenesis, satellite cell activation, myokine and other cytokines modulation and effects of autoantibodies. The interplay of these links may counteract proteolysis and autophagy-related muscle degeneration. The phenomenon is interpreted in the context of I.I. Mechnikov’s idea of the struggle for existence between the cells of the same multi-cellular organism, and in comparison with other examples of organokine-mediated influences on the logistics of the body, when locally produced autacoids serve for re-distribution of resources.

Conclusion. Muscle preservation in some rheumatic autoimmunopathies may result from conflict of local and systemic defensive programs altering metabolic logistics. Understanding this paradox may reveal novel therapeutic insights into tissue preservation, muscle regeneration, and the interplay between immunity and metabolism in chronic autoimmune diseases.

About the authors

Jozélio F. de Carvalho

Federal University of Bahia, Institute of Health Sciences

Author for correspondence.
Email: jotafc@gmail.com
ORCID iD: 0000-0002-7957-0844

Associate Professor, Foreign Fellow of the American College of Rheumatology. M.D., Ph.D

Brazil, Av. Reitor Miguel Calmon, S/N, Vale do Canela, Salvador – BA, ZIP: 40231-300

Leonid P. Churilov

Saint-Petersburg State University

Email: l.churilov@spbu.ru
ORCID iD: 0000-0001-6359-0026

Head of Pathology Department, Institute of Medicine; Associate Professor, Academician of the Academy of Medical Sciences of the Republic of Moldova. M.D., Ph.D

Russian Federation, Universitetskaya nab. 7–9, St. Petersburg, 199034

Roberto Paulo C. de Araujo

Federal University of Bahia, Institute of Health Sciences

Email: rpcaraujo@hotmail.com
ORCID iD: 0009-0004-8214-9040

Professor of the Laboratory of Oral Biochemistry; D.D.M., Ph.D

Brazil, Av. Reitor Miguel Calmon, S/N, Vale do Canela, Salvador – BA, ZIP: 40231-300

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