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Molecular Insights into the Role of Exercise in Disease and Health

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 15 July 2024 | Viewed by 2668

Special Issue Editors


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Guest Editor
Institute of Biomedicine (IBIOMED), University of León, 24007 León, Spain
Interests: biomedical research; exercise physiology; hepatology and gastroenterology; inflammation and oxidative stress

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Guest Editor
Institute of Biomedicine (IBIOMED), University of León, 24007 León, Spain
Interests: molecular biology; physiology; exercise physiology; aging

Special Issue Information

Dear Colleagues,

Physical exercise plays a crucial role in maintaining overall health and preventing the onset of various diseases. The molecular mechanisms underlying the positive effects of exercise, including mind–body practices, on disease prevention and health promotion have been the subject of extensive research in recent years. This Special Issue aims to provide a comprehensive review of the latest advances and discoveries in the field of molecular insights into the role of exercise in disease and health.

Researchers from diverse disciplines have investigated the molecular changes that occur in response to exercise and their impact on disease prevention, treatment, and overall wellbeing. By gathering high-quality contributions from scientists and scholars working in this field, this Special Issue aims to explore the intricate molecular pathways and mechanisms through which exercise exerts its positive effects on human health.

We invite authors to submit original research papers and review articles that explore the molecular signatures of exercise-related processes and their implications for disease prevention, management, and related therapeutic interventions. Manuscripts that focus on the translation of basic molecular knowledge into clinical applications in the context of exercise are highly encouraged. Additionally, articles that investigate the development and application of novel technologies and biomarkers related to exercise and its molecular effects are welcomed.

Topics of interest for this Special Issue include, but are not limited to, the following areas:

  1. Molecular mechanisms underlying the effects of exercise on risk and progression of chronic diseases (e.g., cardiovascular disease, diabetes, obesity, etc.);
  2. Molecular pathways involved in exercise-induced improvements in metabolic health;
  3. Exercise and molecular mechanisms related to neuroprotection and cognitive function;
  4. Molecular insights into exercise-related changes in muscle physiology and performance;
  5. Exercise and molecular regulation of aging processes, with a focus on sarcopenia;
  6. Molecular insights into exercise’s impact on oxidative balance;
  7. Telomeres and their role in disease progression and the aging process;
  8. Exercise-induced modulation of immune functions and inflammation;
  9. Exercise and its effects on mitochondrial biogenesis and functions;
  10. Epigenetic modifications associated with exercise and their impact on gene expression;
  11. Exercise and the effects of circulating biomarkers, such as mRNAs, cfDNA, and exosomes, on disease and health;
  12. The impact of different types of supplementation (e.g., vitamins, polyphenols, etc.) on exercise response in various pathologies;
  13. Molecular insights underlying the physiological adaptations observed due to the practice of mind–body exercises (e.g., Tai Chi, Qi Gong, and Yoga), as well as their potential application in disease prevention and management;
  14. The role of exercise in cancer prevention and treatment, with a focus on molecular mechanisms;
  15. Exercise interventions and personalized medicine, with a focus on molecular profiling and stratification.

Prof. Dr. María José Cuevas-González
Dr. Brisamar Estébanez
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 100 words) can be sent to the Editorial Office for announcement on this website.

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-blind 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

  • physical activity
  • molecular mechanisms
  • disease prevention
  • metabolic health
  • cardiovascular diseases
  • neurodegenerative diseases
  • sarcopenia
  • immune function
  • healthy aging
  • epigenetics

Published Papers (3 papers)

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Research

15 pages, 6269 KiB  
Article
Simultaneous Treatment of 5-Aminosalicylic Acid and Treadmill Exercise More Effectively Improves Ulcerative Colitis in Mice
by Jun-Jang Jin, Il-Gyu Ko, Lakkyong Hwang, Sang-Hoon Kim, Yong-Seok Jee, Hyeon Jeon, Su Bee Park and Jung Won Jeon
Int. J. Mol. Sci. 2024, 25(10), 5076; https://doi.org/10.3390/ijms25105076 (registering DOI) - 7 May 2024
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Abstract
Ulcerative colitis (UC) is characterized by continuous mucosal ulceration of the colon, starting in the rectum. 5-Aminosalicylic acid (5-ASA) is the main therapy for ulcerative colitis; however, it has side effects. Physical exercise effectively increases the number of anti-inflammatory and anti-immune cells in [...] Read more.
Ulcerative colitis (UC) is characterized by continuous mucosal ulceration of the colon, starting in the rectum. 5-Aminosalicylic acid (5-ASA) is the main therapy for ulcerative colitis; however, it has side effects. Physical exercise effectively increases the number of anti-inflammatory and anti-immune cells in the body. In the current study, the effects of simultaneous treatment of treadmill exercise and 5-ASA were compared with monotherapy with physical exercise or 5-ASA in UC mice. To induce the UC animal model, the mice consumed 2% dextran sulfate sodium dissolved in drinking water for 7 days. The mice in the exercise groups exercised on a treadmill for 1 h once a day for 14 days after UC induction. The 5-ASA-treated groups received 5-ASA by enema injection using a 200 μL polyethylene catheter once a day for 14 days. Simultaneous treatment improved histological damage and increased body weight, colon weight, and colon length, whereas the disease activity index score and collagen deposition were decreased. Simultaneous treatment with treadmill exercise and 5-ASA suppressed pro-inflammatory cytokines and apoptosis following UC. The benefits of this simultaneous treatment may be due to inhibition on nuclear factor-κB/mitogen-activated protein kinase signaling activation. Based on this study, simultaneous treatment of treadmill exercise and 5-ASA can be considered as a new therapy of UC. Full article
(This article belongs to the Special Issue Molecular Insights into the Role of Exercise in Disease and Health)
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19 pages, 26924 KiB  
Article
Myokine Secretion following an Aerobic Exercise Intervention in Individuals with Type 2 Diabetes with or without Exercise Resistance
by Léa Garneau, Erin E. Mulvihill, Steven R. Smith, Lauren M. Sparks and Céline Aguer
Int. J. Mol. Sci. 2024, 25(9), 4889; https://doi.org/10.3390/ijms25094889 - 30 Apr 2024
Viewed by 396
Abstract
Type 2 diabetes (T2D) is characterized by muscle metabolic dysfunction that exercise can minimize, but some patients do not respond to an exercise intervention. Myokine secretion is intrinsically altered in patients with T2D, but the role of myokines in exercise resistance in this [...] Read more.
Type 2 diabetes (T2D) is characterized by muscle metabolic dysfunction that exercise can minimize, but some patients do not respond to an exercise intervention. Myokine secretion is intrinsically altered in patients with T2D, but the role of myokines in exercise resistance in this patient population has never been studied. We sought to determine if changes in myokine secretion were linked to the response to an exercise intervention in patients with T2D. The participants followed a 10-week aerobic exercise training intervention, and patients with T2D were grouped based on muscle mitochondrial function improvement (responders versus non-responders). We measured myokines in serum and cell-culture medium of myotubes derived from participants pre- and post-intervention and in response to an in vitro model of muscle contraction. We also quantified the expression of genes related to inflammation in the myotubes pre- and post-intervention. No significant differences were detected depending on T2D status or response to exercise in the biological markers measured, with the exception of modest differences in expression patterns for certain myokines (IL-1β, IL-8, IL-10, and IL-15). Further investigation into the molecular mechanisms involving myokines may explain exercise resistance with T2D; however, the role in metabolic adaptations to exercise in T2D requires further investigation. Full article
(This article belongs to the Special Issue Molecular Insights into the Role of Exercise in Disease and Health)
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18 pages, 3066 KiB  
Article
Endurance Exercise Training Mitigates Diastolic Dysfunction in Diabetic Mice Independent of Phosphorylation of Ulk1 at S555
by Yuntian Guan, Mei Zhang, Christie Lacy, Soham Shah, Frederick H. Epstein and Zhen Yan
Int. J. Mol. Sci. 2024, 25(1), 633; https://doi.org/10.3390/ijms25010633 - 3 Jan 2024
Viewed by 1377
Abstract
Millions of diabetic patients suffer from cardiovascular complications. One of the earliest signs of diabetic complications in the heart is diastolic dysfunction. Regular exercise is a highly effective preventive/therapeutic intervention against diastolic dysfunction in diabetes, but the underlying mechanism(s) remain poorly understood. Studies [...] Read more.
Millions of diabetic patients suffer from cardiovascular complications. One of the earliest signs of diabetic complications in the heart is diastolic dysfunction. Regular exercise is a highly effective preventive/therapeutic intervention against diastolic dysfunction in diabetes, but the underlying mechanism(s) remain poorly understood. Studies have shown that the accumulation of damaged or dysfunctional mitochondria in the myocardium is at the center of this pathology. Here, we employed a mouse model of diabetes to test the hypothesis that endurance exercise training mitigates diastolic dysfunction by promoting cardiac mitophagy (the clearance of mitochondria via autophagy) via S555 phosphorylation of Ulk1. High-fat diet (HFD) feeding and streptozotocin (STZ) injection in mice led to reduced endurance capacity, impaired diastolic function, increased myocardial oxidative stress, and compromised mitochondrial structure and function, which were all ameliorated by 6 weeks of voluntary wheel running. Using CRISPR/Cas9-mediated gene editing, we generated non-phosphorylatable Ulk1 (S555A) mutant mice and showed the requirement of p-Ulk1at S555 for exercise-induced mitophagy in the myocardium. However, diabetic Ulk1 (S555A) mice retained the benefits of exercise intervention. We conclude that endurance exercise training mitigates diabetes-induced diastolic dysfunction independent of Ulk1 phosphorylation at S555. Full article
(This article belongs to the Special Issue Molecular Insights into the Role of Exercise in Disease and Health)
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