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Mitochondrial Origins of Preeclampsia

Award Number: F32HD123271
ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 02/01/2027
PERIOD OF PERFORMANCE END DATE: 01/31/2028

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Mitochondrial Origins of Preeclampsia - PROJECT SUMMARY Preeclampsia (PE) is a complex, multisystem vascular disorder of placental origin, affecting 8.5 million pregnancies worldwide each year. PE and its frequent complication, fetal growth restriction (FGR), pose acute threats to maternal and fetal survival and raise the lifetime risk of cardiovascular disease in affected women by two to tenfold. No effective prevention strategies exist, largely due to a limited understanding of the mechanisms underlying their etiology. Evidence points to placental mitochondrial dysfunction as a central driver. In PE, chronic placental ischemia-reperfusion driven by impaired vasodilation of the uteroplacental arteries disrupts mitochondrial function and architecture, impairing cellular energy production and increasing mitochondrial reactive oxygen species (mtROS) production. Knowledge gaps remain regarding how mitochondrial network architecture and oxidative capacity regulate vascular function, and whether these represent therapeutic targets. Our goal is to determine how placental mitochondrial network architecture and oxidative capacity interact to regulate uteroplacental vascular function in PE and ultimately FGR. In a high-altitude (HA) cohort, where PE incidence is 3-fold greater than at lower altitudes, we found lower placental mitochondrial oxidative metabolism (OXPHOS) in PE vs. controls, with pilot studies implicating defective fatty acid oxidation (FAO) as the primary driver. We hypothesize that placental hypoxia blunts FAO, promoting mitochondrial network fragmentation and elevated mtROS, which in turn increase uteroplacental-fetoplacental vascular resistance and precipitate PE. Aim 1 quantifies placental FAO-linked OXPHOS and mtROS production using high-resolution assays. Aim 2 defines mitochondrial network disruptions using machine-learning 3D imaging of mitochondrial morphology and single- nuclei RNA sequencing. Aim 3 integrates metabolic and morphological data with uteroplacental vascular function measures to test whether FAO deficits and mtROS serve as mechanistic links between placental hypoxia and impaired vascular function, and whether mitochondrial-targeted antioxidants can restore vascular function. This project will provide the first integrated molecular-to-vascular analysis of placental mitochondrial dysfunction in PE. Expected outcomes include identifying FAO impairment as a core metabolic deficit, delineating mitochondrial network signatures that distinguish PE, and proof-of-concept for mitochondrial-targeted therapies. This project directly advances my long-term goal of building a translational research program investigating how mitochondrial physiology drives hypoxia-related cardiovascular and pregnancy disorders. This proposal will provide structured training in clinical and human research, complementing my background in mitochondrial physiology and animal models. By integrating new molecular and analytical approaches, I will gain critical skills to address maternal and fetal vascular health, preparing me to lead innovative, translational investigations.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $79,278 )
2026	2026	THE REGENTS OF THE UNIVERSITY OF COLORADO	13001 E 17TH PL STE F428	AURORA	CO	80045	ADAMS	USA	Child Health and Human Development Extramural Research	000	1	9/2/2026	NEW	$79,278
														Subtotal = $79,278

Grand Total All Awards = $79,278

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Mitochondrial Origins of Preeclampsia

Award Number: F32HD123271

ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 02/01/2027

PERIOD OF PERFORMANCE END DATE: 01/31/2028

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