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Abstract
BackgroundPolyploidization, a process where cells acquire additional chromosome sets, is a unique characteristic of hepatocytes. This process has been increasingly recognized as an adaptive mechanism for maintaining liver function during aging, a period characterized by cellular senescence, DNA damage, and metabolic dysregulation.PurposeThis review explores the molecular mechanisms underlying hepatocyte polyploidization and its potential role in promoting resilience against the aging-related decline in liver function. We assess how polyploid hepatocytes contribute to genomic stability, stress resistance, and metabolic adaptation, highlighting their relevance to liver aging.Main bodyHepatocyte polyploidization occurs through mechanisms such as cytokinesis failure and endoreplication, leading to binuclear or mononuclear polyploid cells. Polyploid hepatocytes exhibit enhanced DNA repair capacity, which helps mitigate the accumulation of age-related genomic damage. The increased gene dosage in polyploid cells facilitates better stress responses, particularly against oxidative stress and genotoxic insults. Metabolic adaptations, including enhanced xenobiotic metabolism and lipid regulation, further support the liver’s ability to maintain homeostasis during aging. Additionally, polyploid cells demonstrate altered epigenetic landscapes and proteostasis mechanisms, contributing to improved cellular function and reduced susceptibility to senescence. These adaptations collectively enhance liver resilience against age-related metabolic and structural challenges.ConclusionHepatocyte polyploidization represents a critical protective mechanism in liver aging, promoting cellular adaptations that safeguard against genomic instability, metabolic dysfunction, and oxidative stress. Understanding the molecular pathways driving polyploidization could pave the way for novel therapeutic strategies to combat age-related liver disorders and enhance health span.Graphical
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