Fatty acid binding proteins-mediated mitochondrial dysfunction in the development of age-related diseases: A review
- PMID: 40203912
- DOI: 10.1016/j.ijbiomac.2025.142913
Fatty acid binding proteins-mediated mitochondrial dysfunction in the development of age-related diseases: A review
Erratum in
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Corrigendum to "Fatty acid binding proteins-mediated mitochondrial dysfunction in the development of age-related diseases: A review" [Int. J. Biol. Macromol. 309 (2025) 142913].Int J Biol Macromol. 2025 Aug;320(Pt 2):146639. doi: 10.1016/j.ijbiomac.2025.146639. Epub 2025 Aug 11. Int J Biol Macromol. 2025. PMID: 40789689 No abstract available.
Abstract
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.
Keywords: Aging; Cardiovascular diseases; FABPs; Metabolic syndromes; Mitochondria; Neurodegenerative diseases; Tumorigenesis.
Copyright © 2025 Elsevier B.V. All rights reserved.
Conflict of interest statement
Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Tianshi Wang reports financial support was provided by National Natural Science Foundation of China. Tianshi Wang reports financial support was provided by Shanghai Jiao Tong University School of Medicine. Xingxing Ren reports financial support was provided by National Natural Science Foundation of China. Xingxing Ren reports financial support was provided by Shanghai Sailing Program. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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