Mitochondrial Metabolic-Signaling Hub in Placenta Accreta Spectrum: From Pathological Reprogramming to Precision Intervention

Rui Wang^1,#, Fangyu Shi^2,#, Bing Zhang^3,*, Tiejun Wang^3,*
1 Department of Clinical Laboratory, Wuxi Maternity and Child Health Care Hospital, Affiliated Women’s Hospital of Jiangnan University, Wuxi, China
2 Department of Clinical Laboratory, Southeast University Affiliated Xuzhou Central Hospital, Xuzhou, China
3 Department of Gynecology, Wuxi Maternity and Child Health Care Hospital, Affiliated Women’s Hospital of Jiangnan University, Wuxi, China
* Corresponding Author: Bing Zhang. Email: email ; Tiejun Wang. Email: email
# These authors contributed equally to this work
(This article belongs to the Special Issue: MitoROS: Exploring Mitochondria and Oxidative Stress)

BIOCELL https://doi.org/10.32604/biocell.2026.083727

Received 09 April 2026; Accepted 21 May 2026; Published online 04 June 2026

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Abstract

Placenta accreta spectrum (PAS) is a severe obstetric complication characterized by pathologically deep trophoblast invasion. Current clinical management relies heavily on reactive surgical interventions due to a lack of early predictive biomarkers and targeted therapies. This review proposes that the mitochondrion serves as the central metabolic-signaling hub driving PAS progression. We systematically analyze how mitochondrial metabolic reprogramming—specifically a Warburg-like shift toward glycolysis—and dysregulated quality control mechanisms promote maladaptive trophoblast phenotypic reprogramming. Central to this process is the “PAS-mitochondria-derived reactive oxygen species (MitoROS)” axis, where MitoROS species act as persistent signal amplifiers promoting epithelial-mesenchymal transition, apoptosis resistance, and impaired vascular remodeling. Furthermore, we explore the crosstalk between mitochondrial dysfunction and the decidual immune microenvironment. By evaluating the potential of cell-free mitochondrial DNA as a circulating biomarker and discussing the prospects of mitochondria-targeted interventions (e.g., MitoQ, SS-31), this synthesis outlines a paradigm shift toward molecular-targeted prevention and precision diagnostics in PAS management.