ReviewFrontiers in cell and developmental biology2026
Biological characteristics of ATP5A1 and its pathogenic mechanisms in human diseases: advances in clinical translation.
Review in Frontiers in cell and developmental biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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8 authors.
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Abstract
ATP5A1 acts as a crucial gene that encodes the core α subunit of the mitochondrial F1-ATPase complex to regulate cellular oxidative phosphorylation (OXPHOS) and maintain energy homeostasis. Consequently, its dysregulation-whether through aberrant expression, genomic alterations, or aberrant post-translational modifications-is hypothesized to be a key potential molecular event contributing to the pathogenesis of malignant tumors, neurodegenerative lesions, and metabolic dysregulation.This review systematically summarizes the molecular structure, biological functions, and regulatory networks of ATP5A1. A comprehensive overview of its expression patterns and pathogenic mechanisms across various diseases, including lung, colorectal, liver, and gastric cancers, as well as non-neoplastic conditions, is provided. Besides, emphasis is placed on the clinical translational potential of ATP5A1 as a diagnostic biomarker and therapeutic target, with recent advances in this area critically evaluated. Furthermore, current challenges and limitations in ATP5A1-related research are discussed, and future directions are proposed to facilitate mechanistic investigations and clinical applications. Collectively, this review establishes a comprehensive theoretical framework for understanding the role of ATP5A1 in disease pathogenesis and supports its potential utility in precision diagnostics and therapeutics.
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