@Article{biocell.2026.083727,
AUTHOR = {Rui Wang, Fangyu Shi, Bing Zhang, Tiejun Wang},
TITLE = {Mitochondrial Metabolic-Signaling Hub in Placenta Accreta Spectrum: From Pathological Reprogramming to Precision Intervention},
JOURNAL = {BIOCELL},
VOLUME = {},
YEAR = {},
NUMBER = {},
PAGES = {{pages}},
URL = {http://www.techscience.com/biocell/online/detail/27091},
ISSN = {1667-5746},
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.},
DOI = {10.32604/biocell.2026.083727}
}