ArticleCellular & molecular biology letters2026
Placental exosomal miR-372-3p drives preeclampsia progression by inducing mitochondrial damage in RVLM neurons.
Article in Cellular & molecular biology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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10 authors.
Funding
Abstract
backgroundPreeclampsia (PE) is a pregnancy-specific disorder rooted in placental dysfunction, characterized by new-onset hypertension with proteinuria and/or end-organ dysfunction, often linked to sympathetic overactivation. The rostral ventrolateral medulla (RVLM) serves as a crucial hub for sympathetic and blood pressure (BP) control. Placental exosomes are implicated in PE, but their role in placenta–RVLM communication is unclear. Investigating this could reveal the neurogenic pathogenesis underlying cardiovascular dysregulation in PE.
methodsPlacental exosomes derived from patients with PE (PE-exo) and normal pregnancies (N-exo) were isolated by ultracentrifugation. Their roles in regulating RVLM neuronal excitability, sympathetic tone, and BP, along with the underlying mechanisms, were evaluated using various experiments.
resultsTail vein injection of PE-exo significantly enhanced RVLM neuronal excitability, sympathetic tone, and BP in pregnant rats. miR-372-3p levels were significantly elevated in PE-exo compared with N-exo and were upregulated in the RVLM of pregnant rats following PE-exo administration. miR-372-3p knockdown reversed the PE-exo-induced increases in RVLM neuronal excitability, sympathetic tone, and BP in pregnant rats. Mechanistically, miR-372-3p markedly reduced MPC1 expression, leading to RVLM neuronal mitochondrial damage.
conclusionsThis study is the first to demonstrate that placental exosomes deliver miR-372-3p to the RVLM neurons, impairing neuronal mitochondrial function and thereby promoting neuronal hyperexcitability, sympathetic overactivity, and elevated BP in PE.
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