Reproductive sciences (Thousand Oaks, Calif.)Jul 20, 2026

Using Data Analysis and Testing to Identify Two Mitophagy-Related Proteins as Diagnostic and Treatment Targets in Polycystic Ovary Syndrome

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Jul 21, 2026

Abstract

Elevated expression of AMFR, FABP5, and HMOX1 was identified in a hyperandrogenism-induced PCOS cell model.

Polycystic Ovary Syndrome (PCOS) is linked to mitochondrial dysfunction, which affects energy metabolism and oxidative stress.
Dysregulated mitophagy is associated with metabolic complications in PCOS, including obesity and inflammation.
Gene expression analysis revealed AMFR, FABP5, and HMOX1 as significant autophagy-related genes in PCOS.
FABP5 and HMOX1 may serve as potential diagnostic targets for PCOS.
High-affinity compounds targeting these genes could be explored as therapeutic options.

Simplified

Polycystic Ovary Syndrome (PCOS) is a heterogeneous endocrine-metabolic disorder characterized by ovulatory dysfunction, hyperandrogenism, and insulin resistance, in which mitochondrial dysfunction has been increasingly implicated. Mitochondria regulate energy metabolism and oxidative stress, with mitophagy maintaining cellular balance. Dysregulated mitophagy relates to PCOS metabolic issues like obesity and inflammation. This study analyzed gene expression datasets to find autophagy-related genes in PCOS, identifying AMFR, FABP5, and HMOX1 as key genes. We built a diagnostic model and confirmed their elevated expression in a hyperandrogenism-induced PCOS cell model, revealing potential small-molecule drugs targeting these genes. Our integrative bioinformatics analysis and systematic molecular experiments suggest that FABP5 and HMOX1 are potential PCOS diagnostic targets, with high-affinity compounds as therapies,highlighting the pathological relevance of mitophagy-related genes in PCOS.

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Using Data Analysis and Testing to Identify Two Mitophagy-Related Proteins as Diagnostic and Treatment Targets in Polycystic Ovary Syndrome

Abstract

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