Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

Journal Browser

Exercise in Health and Diseases: From the Molecular Perspectives

Editors
Special Issue Information
Keywords
Benefits of Publishing in a Special Issue
Published Papers

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (10 September 2026) | Viewed by 4023

Share This Special Issue

Editors

Dr. Nathalia Bernardes

E-Mail Website
Guest Editor

Human Movement Lab, Sao Judas Tadeu University, Sao Paulo 03166-000, Brazil
Interests: cardiology; heart; exercise

Dr. Danielle Dias

E-Mail Website
Guest Editor

Department of Physiology, Federal University of São Paulo, São Paulo, Brazil
Interests: cardiovascular; heart disease; atherosclerosis; hypertension

Special Issue Information

Dear Colleagues,

Physical exercise is widely recognized as a non-pharmacological strategy for health promotion and disease management. However, the molecular mechanisms underlying its systemic benefits remain incompletely understood. This Special Issue aims to explore the molecular, cellular, and physiological pathways through which exercise modulates health and disease processes. We welcome original research articles and reviews addressing the molecular responses to different exercise modalities, including therapeutic exercise, aerobic and resistance training, and exercise interventions applied to special populations. Topics of interest include, but are not limited to, redox balance, inflammation, autonomic nervous system regulation, neuroplasticity, mitochondrial function, metabolic signaling, and interactions between exercise and emerging therapeutic approaches. Both experimental and clinical studies are encouraged, particularly those integrating molecular analyses with functional, physiological, or clinical outcomes. By bringing together multidisciplinary perspectives, this Special Issue seeks to advance the understanding of exercise as a biological stimulus capable of inducing molecular adaptations relevant to disease prevention, treatment, and rehabilitation.

Dr. Nathalia Bernardes
Dr. Danielle Dias
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

exercise physiology
molecular mechanisms of exercise
exercise-induced cellular signaling
metabolic signaling pathways
redox biology and exercise

Benefits of Publishing in a Special Issue

Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

Download All Papers

Order results

Result details

Show export options Show export options

Select all

Export citation of selected articles as:

Research

Jump to: Review

24 pages, 30006 KB

Open AccessArticle

Regular Aerobic Exercise Can Effectively Ameliorate the Skeletal Muscle and Mitochondrial Function Impairments Caused by bves Deficiency in Zebrafish

by Wanwan Cai, Wanbang Zhou, Xiushan Wu, Junrong Lei, Haochen Wang, Qiong Wu, Song Zhou, Kang Sun, Xiuyan Li, Zhilong Zhang, Jisheng Zhang, Jingying Ouyang, Yongqing Li, Zhigang Jiang, Xianchu Liu, Wuzhou Yuan and Lan Zheng

Int. J. Mol. Sci. 2026, 27(12), 5594; https://doi.org/10.3390/ijms27125594 - 20 Jun 2026

Viewed by 496

Abstract

The Popeye domain-containing protein 1 (Popdc1), also known as Bves, plays a crucial role in maintaining skeletal muscle homeostasis, with its variants leading to limb–girdle muscular dystrophy type R25. Skeletal muscles of patients with the homozygous missense variant of Bves exhibit impaired membrane trafficking, while skeletal muscle fibers in bves^S191F homozygous mutant zebrafish are significantly reduced and disorganized. However, the mechanism by which the absence of bves induces skeletal muscle atrophy remains unclear. In this study, we discovered a novel mechanism whereby bves deficiency drives skeletal muscle atrophy by disrupting mitochondrial structure and function. Our findings indicate that bves knockout leads to a significant decrease in zebrafish’s ability to swim, atrophy of skeletal muscle tissue, loss of cell membrane localization signals, and abnormalities in mitochondrial structure and function. After an 8-week intervention of regular aerobic exercise, the symptoms of skeletal muscle atrophy in bves knockout zebrafish were significantly alleviated, and the expression levels of genes and proteins related to mitochondrial were effectively rescued. These findings establish a connection between bves deficiency-induced disruption of mitochondrial structure and function and the onset and progression of skeletal muscle tissue atrophy symptoms, thereby laying a molecular foundation for exercise rehabilitation strategies in atrophic myopathy. Full article

(This article belongs to the Special Issue Exercise in Health and Diseases: From the Molecular Perspectives)

► Show Figures

Figure 1

14 pages, 8659 KB

Open AccessArticle

Exercise Improves Atherosclerotic Plaque Stability Through Macrophage Autophagy and the FGF21 Signaling Pathway

by Qingbo Li, Weidong Mao, Yao Lu, Tianrui Lu, Xiaonan Xu, Yibin Pan, Sang Ki Lee, Lifeng Wang, Ting Li, Jinming Zhou, Wei Li and Mallikarjuna Korivi

Int. J. Mol. Sci. 2026, 27(11), 4996; https://doi.org/10.3390/ijms27114996 - 30 May 2026

Cited by 1 | Viewed by 613

Abstract

Atherosclerosis (AS) is a major driver of acute cardiovascular events, yet the mechanisms by which exercise stabilizes atherosclerotic plaque remain poorly understood. This study investigated the protective effects of a 12-week treadmill exercise training on plaque stability and macrophage autophagy in ApoE^−/− mice fed an atherogenic diet. Exercise significantly decreased the serum pro-inflammatory cytokine (tumor necrosis factor-α) and increased the anti-inflammatory (interleukin-10) mediator in AS mice. Histopathology analysis revealed that exercise improved plaque stability through reduced necrotic core size, increased fibrous cap thickness, and increased collagen content. These improvements were accompanied by decreased lipid accumulation, MMP-9 expression, and macrophage infiltration (CD11b) within the plaque. Mechanistically, exercise activated plaque autophagy, evidenced by increased LC3B fluorescence, elevated LC3II/I ratio, restoration of Beclin-1, and degradation of p62. Notably, exercise-induced autophagy is specific to plaque-resident macrophages, as demonstrated by strong colocalization of LC3B and CD11b fluorescent signals (Pearson’s correlation coefficient = 0.56). Furthermore, exercise restored fibroblast growth factor 21 (FGF21) levels in both circulation and plaque while concurrently suppressing downstream PI3K/Akt/mTOR signaling. Collectively, these findings demonstrated that exercise promotes plaque stability by reducing lipid accumulation, macrophage infiltration, MMP-9 expression, and activation of FGF21. This protection is likely mediated by the activation of macrophage autophagy, specific to plaque-resident macrophages, indicating the cardioprotective benefits of aerobic exercise against AS. Full article

(This article belongs to the Special Issue Exercise in Health and Diseases: From the Molecular Perspectives)

► Show Figures

Figure 1

Review

Jump to: Research

21 pages, 1382 KB

Open AccessReview

Precision Cardiogenomics in Athletes

by Pari Goyal, Alwaleed Aljohar, Reid A. Mitchell, Nathaniel Moulson, James McKinney, Saul Isserow and Zachary Laksman

Int. J. Mol. Sci. 2026, 27(12), 5250; https://doi.org/10.3390/ijms27125250 - 10 Jun 2026

Viewed by 792

Abstract

Sudden cardiac death (SCD) in athletes often represents the first manifestation of an underlying inherited cardiovascular disorder exposed by adrenergic stress, altered calcium cycling, mechanical loading, and metabolic demand during intense exercise. This review focuses on the molecular architecture that links genotype to arrhythmogenic phenotype in athletes, emphasizing sarcomeric force generation and energetic inefficiency in hypertrophic cardiomyopathy, desmosomal failure and Hippo/Wnt/transforming growth factor-beta (TGF-β) signaling in arrhythmogenic cardiomyopathy, and ion-channel and calcium/calmodulin-dependent protein kinase II (CaMKII)calcium handling abnormalities in inherited channelopathies. This review further examines how exercise-induced physiological remodeling intersects with these pathways through insulin-like growth factor-1 (IGF-1)/phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT) signaling, mitochondrial biogenesis, oxidative stress, inflammatory signaling, and epigenetic regulation. Attention is given to the molecular basis of genotype-positive/phenotype-negative states, variable penetrance, and exercise-mediated disease expression. Finally, the integration of molecular biology with genomic data, polygenic risk, and emerging digital phenotyping is discussed to refine mechanism-based risk stratification and identify future therapeutic targets for prevention of SCD in athletes. Full article

(This article belongs to the Special Issue Exercise in Health and Diseases: From the Molecular Perspectives)

► Show Figures

Figure 1

27 pages, 1965 KB

Open AccessReview

Molecular Biomarkers of Training Responses: A Systems Framework for Exercise Adaptation and Athlete Monitoring

by Dan Cristian Mănescu, Andreea Voinea, Camelia Daniela Plastoi, Alexandra Reta Iacobini, Alina Anca Vulpe, Ancuța Pîrvan, Corina Claudia Dinciu, Bogdan Iulian Vulpe, Cristian Băltărețu and Adrian Iacobini

Int. J. Mol. Sci. 2026, 27(8), 3601; https://doi.org/10.3390/ijms27083601 - 17 Apr 2026

Cited by 7 | Viewed by 1472

Abstract

Exercise adaptation depends on overload that is resolved by recovery, yet the same biology becomes maladaptive when immune, endocrine, metabolic, and muscle-centered stress signals fail to normalize. Exercise-induced maladaptation represents a systems-level failure of biological resolution, with direct relevance to disease-like dysregulation. Functional overreaching, non-functional overreaching, and overtraining syndrome remain difficult to diagnose because no single biomarker provides adequate specificity, temporal stability, or clinical portability. This narrative review synthesizes human and mechanistic evidence across proteomics, transcriptomics, metabolomics, endocrine profiling, extracellular vesicles, and mitochondrial quality-control biology to define the molecular architecture most relevant to athlete monitoring. Across these layers, the most coherent signatures cluster in immune-acute-phase activation, redox-buffering strain, endocrine drift, altered substrate availability, excitation–contraction dysfunction, integrated stress-response signaling, and defects in autophagy–mitophagy and lysosomal remodeling. Three translational elements emerge from this synthesis: a systems-convergence model of recovery failure, a staged biomarker deployment hierarchy, and a provisional recovery failure index. The practical priority is therefore not a solitary marker, but serial phenotype-anchored multimarker panels that connect circulating signals with muscle-centered biology and support decision-making before prolonged recovery failure becomes entrenched. Full article

(This article belongs to the Special Issue Exercise in Health and Diseases: From the Molecular Perspectives)

► Show Figures

Journal Menu

Journal Browser

Exercise in Health and Diseases: From the Molecular Perspectives

Share This Special Issue

Editors

Special Issue Information

Keywords

Benefits of Publishing in a Special Issue

Published Papers (4 papers)

Research

Review

Further Information

Guidelines

MDPI Initiatives

Follow MDPI