🧬 BDNF Extraction Viewer

Извлечено: 997 / 997 (100.0%) Средняя confidence: 0.13
← Назад к списку

Exercise-Induced Molecular Adaptations in Chronic Non-Communicable Diseases-Narrative Review.

PMID: 41465520 · DOI: 10.3390/ijms262412096 · International journal of molecular sciences, 2025 · Héctor Fuentes-Barría, Raúl Aguilera-Eguía, Miguel Alarcón-Rivera, Olga López-Soto, Juan Alberto Aristizabal-Hoyos, Ánge
📄 Abstract

Physical exercise is a potent non-pharmacological strategy for the prevention and management of chronic non-communicable diseases (NCDs), including type 2 diabetes, cardiovascular diseases, obesity, and certain cancers. Growing evidence demonstrates that the benefits of exercise extend beyond its physiological effects and are largely mediated by coordinated molecular and cellular adaptations. This review synthesizes current knowledge on the key mechanisms through which exercise modulates metabolic health, emphasizing intracellular signaling pathways, epigenetic regulation, and myokine-driven inter-organ communication. Exercise induces acute and chronic activation of pathways such as AMPK, PGC-1α, mTOR, MAPKs, and NF-κB, leading to enhanced mitochondrial biogenesis, improved oxidative capacity, refined energy sensing, and reduced inflammation. Additionally, repeated muscle contraction stimulates the release of myokines-including IL-6, irisin, BDNF, FGF21, apelin, and others-that act through endocrine and paracrine routes to regulate glucose and lipid metabolism, insulin secretion, adipose tissue remodeling, neuroplasticity, and systemic inflammatory tone. Epigenetic modifications and exercise-responsive microRNAs further contribute to long-term metabolic reprogramming. Collectively, these molecular adaptations establish exercise as a systemic biological stimulus capable of restoring metabolic homeostasis and counteracting the pathophysiological processes underlying NCDs. Understanding these mechanisms provides a foundation for developing targeted, personalized exercise-based interventions in preventive and therapeutic medicine.

Confidence: 0.12 · 4 полей извлечено
Идентификация (6 полей)
Механизм действия (21 полей)
Mechanism
0.00
Mutations (obesity/lean)
0.00
Activity (obesity)
0.00
Activity temporal
0.00
Energy balance
0.00
Appetite
0.00
Fat metabolism
0.00
Lipolysis
0.00
Thermogenesis
0.00
Muscle metabolism
0.00
Inflammation
0.00
Glucose metabolism
0.00
AA metabolism
0.00
Hormonal pathways
0.00
Cell death
0.00
Adipocyte fibrosis
0.00
Upstream (biochem)
0.00
Upstream (physiol)
0.00
Downstream (biochem)
0.00
Downstream (physiol)
0.00
PTMs
0.00
Экспрессия (8 полей)
Tissue expression
0.00
In vitro
0.00
In vivo
Exercise-induced molecular adaptations studied in humans and animal models (rats, mice) including high-fat diet-induced obesity models.
0.90
In silico
0.00
Genetic association
APOE genotype-dependent effects on exercise mitigation of cardiac dysfunction mentioned.
0.80
Ex vivo
0.00
Animal model
High-fat diet-induced obesity rat model; adult mice; mouse skeletal muscle and adipose tissue.
0.90
Diet/model
High-fat diet; intermittent fasting; short-term nutrient-exercise stress.
0.90
Клиника (11 полей)