The DOI matches its Crossref record; 120 of the 120 references it cites were found in a registry or an index.
CPT1A-mediated Fat Oxidation, Mechanisms, and Therapeutic Potential
Abstract
Energy homeostasis during fasting or prolonged exercise depends on mitochondrial fatty acid oxidation (FAO). This pathway is crucial in many tissues with high energy demand and its disruption results in inborn FAO deficiencies. More than 15 FAO genetic defects have been currently described, and pathological variants described in circumpolar populations provide insights into its critical role in metabolism. The use of fatty acids as energy requires more than 2 dozen enzymes and transport proteins, which are involved in the activation and transport of fatty acids into the mitochondria. As the key rate-limiting enzyme of FAO, carnitine palmitoyltransferase I (CPT1) regulates FAO and facilitates adaptation to the environment, both in health and in disease, including cancer. The CPT1 family of proteins contains 3 isoforms: CPT1A, CPT1B, and CPT1C. This review focuses on CPT1A, the liver isoform that catalyzes the rate-limiting step of converting acyl-coenzyme As into acyl-carnitines, which can then cross membranes to get into the mitochondria. The regulation of CPT1A is complex and has several layers that involve genetic, epigenetic, physiological, and nutritional modulators. It is ubiquitously expressed in the body and associated with dire consequences linked with genetic mutations, metabolic disorders, and cancers. This makes CPT1A an attractive target for therapeutic interventions. This review discusses our current understanding of CPT1A expression, its role in heath and disease, and the potential for therapeutic opportunities targeting this enzyme.
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Cites
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Cited by
Mitochondrial CPT1A: Insights into structure, function, and basis for drug development
Liang, K. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1160440 · Cited by 156
“CPT1A is a significant therapeutic target due to its important function in a variety of illnesses (Schlaepfer and Joshi, 2020).”
BackgroundLinking Metabolic Reprogramming, Plasticity and Tumor Progression
Shuvalov, O., Daks, A., Fedorova, O., Petukhov, A., & Barlev, N. (2021) · Cancers · doi:10.3390/cancers13040762 · Cited by 63
Acetyl-CoA metabolism as a therapeutic target for cancer
Chen, G., Bao, B., Cheng, Y., Tian, M., Song, J., Zheng, L., & Tong, Q. (2023) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2023.115741 · Cited by 54
Joshi, M., Kim, J., D’Alessandro, A., Monk, E., Bruce, K., Elajaili, H., Nozik-Grayck, E., Goodspeed, A., Costello, J. C., & Schlaepfer, I. R. (2020) · Cancers · doi:10.3390/cancers12113431 · Cited by 54
Self-citationAcylated Ghrelin as a Multi-Targeted Therapy for Alzheimer's and Parkinson's Disease
Reich, N., & Hölscher, C. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.614828 · Cited by 48
Metadata
- Authors
- Schlaepfer, I. R., & Joshi, M.
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2020-01-04
- Volume
- 161
- Issue
- 2
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2997840987
- Cited by
- 732
- References
- 120
- FWCI
- 40.13
- Type
- journal article
- Language
- en
- Open access
- closed
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