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Fatty acid-binding proteins (FABPs) act as lipid chaperones and play a role in the pathological processes of various lipid signaling pathways. Mitochondria are crucial for the regulation of lipid metabolism. As an aging marker, lipid-mediated mitochondrial dysfunction has been observed in the etiology of numerous diseases, including neurodegenerative diseases, metabolic syndromes, cardiovascular diseases, and tumorigenesis. Members of the FABP family have been identified to regulate mitochondrial function. Targeting FABPs specifically may provide a promising approach to improve mitochondrial function and treat age-related diseases. This review summarizes the connection between FABPs and mitochondrial function and highlights certain FABPs involved in age-related diseases that hold significant therapeutic promise.
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http://dx.doi.org/10.1016/j.ijbiomac.2025.142913 | DOI Listing |
J Orthop Res
September 2025
Institute of Orthopaedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Osteoporotic hip fractures are a considerable cause of pain and disability particularly among the elderly. Osteoporosis causes loss of bone stability, which in turn leads to an increased risk of fractures especially in metaphyseal bone. Moreover, the body's capacity for healing is diminished, resulting in prolonged recovery times following these fractures.
View Article and Find Full Text PDFCytokine Growth Factor Rev
September 2025
Shandong University of Traditional Chinese Medicine, Jinan 250355, China; The Second Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250001, China. Electronic address:
This review summarizes the biological properties of key myokines (Irisin, Apelin, CLCF1, and Myostatin) and osteokines (Osteocalcin, Sclerostin, FGF23 and the RANKL/OPG system). This work provides an in-depth analysis of the age-related network imbalance mechanism characterized by "downregulation of protective factors (Irisin, CLCF1, and uncarboxylated Osteocalcin) - upregulation of pro-degenerative factors (Myostatin, Sclerostin, and FGF23) - inflammation-driven amplification", and reveals the mechanism by which this network imbalance contributes to the comorbidity of sarcopenia, osteoporosis, and neurodegenerative diseases. Furthermore, the review evaluates the intersecting regulatory networks and molecular pathways through which myo-osteogenic factors modulate neurotrophic factors (BDNF, NGF and GDNF), and proposes intervention strategies based on these intersecting regulatory networks.
View Article and Find Full Text PDFExp Eye Res
September 2025
School of Basic Medicine, Qingdao University, Qingdao, Shandong Province, 266071, China; Department of Ophthalmology, Qingdao Eighth People's Hospital, Qingdao, Shandong Province, 266121, China; Institute of Stem Cell Regeneration Medicine, School of Basic Medicine, Qingdao University, Qingdao, Shan
Mitochondria play a crucial role in energy production and are intimately associated with ocular function. Mitochondrial dysfunction can trigger oxidative stress and inflammation, adversely affecting key ocular structures such as the lacrimal gland, lens, retina, and trabecular meshwork. This dysfunction may compromise the barrier properties of the trabecular meshwork, impeding aqueous humour outflow, elevating intraocular pressure, and resulting in optic nerve damage and primary open-angle glaucoma.
View Article and Find Full Text PDFJ Med Internet Res
September 2025
Department of Internal Medicine, Seoul National University College of Medicine, 101 Daehak-ro, Jongno-gu, Seoul, 03080, Republic of Korea, 82 0220721965.
Background: Biological age (BA) is increasingly recognized as a valuable alternative to chronological age (CA) for assessing an individual's health and aging status. However, existing models are based on limited clinical parameters and have not thoroughly integrated morbidity and mortality data.
Objective: This study aimed to develop and validate a novel transformer-based model, referred to as the BA - CA gap model, for BA estimation that incorporates morbidity and mortality information to improve predictive accuracy and enhance clinical use in the early identification of the risk of age-related diseases.
PLoS One
September 2025
MRC Epidemiology Unit, University of Cambridge School of Clinical Medicine, Institute of Metabolic Science, Cambridge Biomedical Campus, Cambridge, United Kingdom.
Background: Many young people fail to achieve the minimum recommended amount of physical activity to benefit their health. Understanding the nature of age-related changes in behaviour and how this varies for population sub-groups is informative for intervention design. The aim of this study was to describe age-related changes in physical activity and sedentary time and examine variability in patterns of change across demographic sub-groups.
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