Impact of Lifestyle Changes on Biomolecular Profiles Across the Lifespan

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Chemical Biology".

Deadline for manuscript submissions: 30 December 2026 | Viewed by 893

Special Issue Editors


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Guest Editor
Department of Health Sciences, European University Miguel de Cervantes, Valladolid, Spain
Interests: exercise physiology

E-Mail Website
Guest Editor
i+HeALTH Strategic Research Group, Department of Health Sciences, Miguel de Cervantes European University (UEMC), 47012 Valladolid, Spain
Interests: exercise metabolism; exercise biochemistry
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Special Issue Information

Dear Colleagues,

Lifestyle factors, including diet, physical activity, sleep, stress management, and environmental exposures, are key modulators of health across the human lifespan. These elements influence biomolecular pathways that underlie physiological adaptation, disease susceptibility, and healthy aging. In particular, molecular regulators such as microRNAs play an important role in mediating the effects of lifestyle on gene expression, inflammation, metabolism, and cellular function. Dysregulation of these pathways is closely linked to the onset and progression of major chronic diseases, including cardiovascular disease, diabetes, obesity, neurodegenerative disorders, and cancer.

This Special Issue aims to gather high-quality research and reviews on how lifestyle factors shape biomolecular profiles with a particular emphasis on disease-related mechanisms. We especially welcome studies addressing the role of microRNAs, hormonal regulation, and other molecular mediators that connect lifestyle with health outcomes across different stages of life. Submissions may include experimental studies, preclinical investigations, and integrative reviews.

Dr. Sergio Maroto-Izquierdo
Dr. Kayvan Khoramipour
Guest Editors

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Keywords

  • lifestyle
  • microRNAs
  • disease

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Published Papers (1 paper)

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Research

16 pages, 1051 KB  
Article
High-Intensity Interval and Aerobic Training Alleviate Cardiac Pathology, Apoptosis, and Atrial Fibrillation in Rats with Chronic Kidney Disease: The Roles of FGF23 and Klotho
by Sina Rokhsati, Nazanin Shahsavari, Shahram Rabbani, Katsuhiko Suzuki and Kayvan Khoramipour
Biomolecules 2026, 16(4), 513; https://doi.org/10.3390/biom16040513 - 30 Mar 2026
Viewed by 626
Abstract
Chronic kidney disease (CKD) leads to metabolic and cardiovascular complications, and the dysregulation of key biomolecules, namely fibroblast growth factor 23 (FGF23) and Klotho, plays a central role. This study investigated the effects of high-intensity interval training (HIIT) and moderate aerobic training (AT) [...] Read more.
Chronic kidney disease (CKD) leads to metabolic and cardiovascular complications, and the dysregulation of key biomolecules, namely fibroblast growth factor 23 (FGF23) and Klotho, plays a central role. This study investigated the effects of high-intensity interval training (HIIT) and moderate aerobic training (AT) on FGF23, Klotho, mineral metabolism, apoptosis markers (BAX, Bcl2), and atrial fibrillation (AF) in a rat CKD model. The study used 35 Wistar rats randomly assigned to control (CTL), sham (SH), CKD, CKD + HIIT, and CKD + AT groups. CKD was induced by 5/6 nephrectomy surgery. Exercise interventions consisted of eight weeks of HIIT (80–100% of maximum speed, 24–54 min/week) or AT (45–55% of maximum speed, 40–60 min/week), conducted three times weekly on a treadmill. We measured heart weight, blood levels of FGF23, Klotho, and mineral metabolism markers, as well as the heart expression of apoptosis proteins (i.e., BAX, Bcl2) and atrial fibrillation (AF). Both exercise types reduced the heart weight and heart/body weight ratio; attenuated CKD-induced elevations in FGF23 and reductions in Klotho; improved blood levels of phosphate, PTH, and vitamin D; and modulated apoptotic markers by decreasing BAX and increasing Bcl2 levels. Exercise improved cardiac function and reduced the AF duration. These findings emphasize that exercise could be a helpful non-pharmacological intervention to ameliorate CKD-induced cardiovascular and metabolic disturbances through the modulation of the FGF23 and Klotho pathways. Full article
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