Molekulyarnaya Meditsina (Molecular medicine)Molekulyarnaya Meditsina (Molecular medicine)Молекулярная медицина1728-29182499-9490Russkiy Vrach Publishing House71723710.29296/24999490-2026-04-10xfogveReviewsОбзорыReview ArticleAbsence of muscle atrophy in some rheumatic diseases: fundamental and applied aspects of paradoxical preservation of inflammatory musclesОтсутствие мышечной атрофии при некоторых ревматических заболеваниях: фундаментальные и прикладные аспекты парадоксальной сохранности воспаленных мышцhttps://orcid.org/0000-0002-7957-0844de CarvalhoJozélio F.де КарвальюЖозелиу Фрейре
Brazil

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

доцент кафедры клинической медицины, иностранный член Американской коллегии ревматологии. Доктор медицины, доктор философии

jotafc@gmail.comhttps://orcid.org/0000-0001-6359-0026ChurilovLeonid P.ЧуриловЛеонид Павлович
Russian Federation

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

доцент, заведующий кафедрой патологии Медицинского института, академик Академии медицинских наук Республики Молдова. Кандидат медицинских наук

l.churilov@spbu.ruhttps://orcid.org/0009-0004-8214-9040de AraujoRoberto Paulo C.де АраужуРоберту Паулу Коррейя
Brazil

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

профессор лаборатории биохимии полости рта; Доктор стоматологии, доктор философии

rpcaraujo@hotmail.comFederal University of Bahia, Institute of Health SciencesФедеральный университет Байи, Институт наук о здоровьеSaint-Petersburg State UniversityСанкт-Петербургский государственный университетru13082026202624471801208202612082026Received:12082026Accepted:12082026Published:13082026Copyright ©; 2026, Russkiy Vrach Publishing HouseCopyright ©; 2026, ИД "Русский врач"2026Russkiy Vrach Publishing HouseИД "Русский врач"https://journals.eco-vector.com/1728-2918/article/view/717237

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.

Введение. Хотя хроническое воспаление обычно связано с усилением катаболизма и истощением тканей, большинство аутоиммунных ревматических заболеваний, включая полимиозит, дерматомиозит, волчаночный миозит и смешанные миопатии, как правило, парадоксальным образом демонстрируют сохранение трофики мышц, несмотря на их значительную слабость и патогистологические признаки воспаления. Один лишь миозит с включениями обычно характеризуется прогрессирующей и необратимой атрофией мышц.

Цель: сформулировать гипотезу о том, что уникальное иммунометаболическое равновесие при ревматических миопатиях поддерживает мышечную массу, несмотря на воспаление, и представить обзорные данные в поддержку этой гипотезы.

Материал и методы. Проанализированы библиографические базы данных PubMed/MedLine, Embase, eLibrary.ru и Scielo на предмет статей по запросам «Ревматические заболевания» И «Сохранение мышц», а также по запросам «Сохранение мышц» И «Органокины» ИЛИ «Цитокины» за период с 1965 по 2025 год, без каких-либо языковых ограничений.

Обсуждаются возможные механизмы, включающие митохондриальный биогенез, активацию сателлитных клеток, модуляцию миокинами и другими цитокинами, а также эффекты аутоантител. Взаимодействие этих звеньев может противодействовать дегенерации мышц, связанной с протеолизом и аутофагией. Данное явление интерпретируется в контексте идей И.И. Мечникова о борьбе за существование между клетками одного и того же многоклеточного организма, а также в сравнении с другими примерами опосредованного органокинами влияния на логистику организма, когда локально продуцируемые аутакоиды служат перераспределению ресурсов.

Заключение. Сохранение мышечной массы при некоторых ревматических аутоиммунных заболеваниях может быть результатом конфликта между местными и системными защитными механизмами, изменяющего метаболическую логистику. Понимание этого парадокса может открыть новые терапевтические возможности в области сохранения тканей, регенерации мышц и иммунометаболических взаимодействий при хронических аутоиммунных заболеваниях.

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