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Life sciences · Review
Journal of Biomolecules Pathogenesis and Therapeutics · September 17, 2026
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Background: Mitochondrial metabolic reprogramming by Oxidative phosphorylation (OXPHOS) and Fatty acid oxidation (FAO) has become survival and therapy-resistance driver in acute myeloid leukemia (AML) and pancreatic ductal adenocarcinoma (PDAC). This review aimed to evaluate the role of OXPHOS and FAO pathways in cancers and potential as therapeutic targets. Methods: The research was conducted according to PRISMA 2020 guidelines. PubMed, Scopus, Web of Science, and Google Scholar databases were searched from January 2013 to December 2025. Articles with data on effect of pharmacological or genetic inhibition of OXPHOS and FAO in AML and PDAC were considered. Reviews, case reports, and non-English articles were excluded. The SYRCLE and OHAT tools were used to determine the risk of bias, and the certainty of evidence was determined using GRADE. MetaAnalysisOnline Tool was used for statistical analysis. Results: Sixteen studies met inclusion criteria. Studies included in AML assessed OXPHOS (SMD = -0.76, 95% CI: -3.18 to -1.67, p= 0.05) and FAO (SMD = -0.19, 95% CI: -7.31 to -6.93, p> 0.05) showed no significant differences and high heterogeneity (I2 > 94%). In PDAC, four studies provided data on OXPHOS (SMD = -5.27, 95% CI: -15.59 to -5.05, p.05) and four on FAO (SMD = -215.42, 95% CI: -616.27 to -185.44, p>0.05) and high heterogeneity (I² > 95%). The overall risk of bias was low to moderate, and certainty of evidence was moderate. Conclusion: In cancer cells, AML, and PDAC, OXPHOS and FAO were parallel dependent pathways, making mitochondrial metabolism a promising target therapy.