Eghbali Research Lab

Group in lab coats standing in front of David Geffen School of Medicine sign

Eghbali Lab

Studying heart failure, pulmonary hypertension, the role of micro-RNAs, & more.

About the PI

Headshot of Dr. Mansoureh Eghbali

Full Biography

Dr. Mansoureh Eghbali

Dr. Eghbali is a Professor in the Department of Anesthesiology and Perioperative Medicine at UCLA. She is also Director of Physician-Scientist Training Program, and Director of the Basic Science Training Environment in the department.

She received her Master’s degree in Biomedical Engineering from university of New South Wales in Sydney Australia in 1995 and her PhD degree from the John Curtin School of Medical Research, Australian National University in 1999.

Our Research 

  • Diagram showing how Y-Chromosome gene, Uty, protects against pulmonary hypertension by reducing proinflammatory chemokines
    Graphic showing the proposed mechanism of Uty/Cxcl9/Cxcl10 axis in pulmonary hypertension (PH) pathogenesis. EC = endothelial control; KD = knockdown; KO = knockout; PAH = pulmonary arterial hypertension; PH = pulmonary hypertension.
  • Diagram of two circles showing the role of estrogen receptors in cardiovascular diseases
    Graphical summary of how estrogen receptors α, β, and GPR30 regulate key processes in cardiovascular disease, including ischemia/reperfusion injury, heart failure with reduced ejection fraction, and heart failure with preserved ejection fraction.
  • Diagram with arrows showing how oral 15-HETE induces pulmonary hypertension in mice by triggering T-cell dependent endothelial cell apoptosis
    A 15-HETE diet increases oxidized lipid production by intestinal epithelial cells, activating pulmonary arterial endothelial cells. CD8-positive T cells induce apoptosis of cells, leading to pulmonary hypertension. Transgenic 6F denotes experimental model
  • Circle diagram showing pregnancy-associated cardiac dysfunction and the role of RNAs
    Graphical overview of literature regarding dysregulated microRNAs in patients suffering from pregnancy-related cardiac dysfunction. PE: preeclampsia, GH: gestational hypertension, PPCM: peripartum cardiomyopathy, GDM: gestational diabetes mellitus.
  • Diagram showing connecting sex-differences signaling, and microRNAs in cardiac fibrosis
    Graphical summary of estrogen signaling in cardiac fibroblasts, where estrogen receptors directly or indirectly regulate fibrosis-related gene expression through transcriptional and signaling pathways.
  • Diagram showing the protective role of estrogen receptors in cardiovascular disease
    Schematic showing how estrogen (E2) regulates gene expression and signaling via genomic and non-genomic pathways, and enhances mitochondrial function through mitochondrial estrogen receptors.
  • Diagram showing role of oxidized lipids in pulmonary arterial hypertension
    Hypothetical model showing that linoleic and arachidonic acids are oxidized into HETEs and HODEs in pulmonary artery cells, promoting inflammation in pulmonary arterial hypertension. The peptide 4F inhibits their production.
  • Diagram showing how Y-Chromosome gene, Uty, protects against pulmonary hypertension by reducing proinflammatory chemokines
  • Diagram of two circles showing the role of estrogen receptors in cardiovascular diseases
  • Diagram with arrows showing how oral 15-HETE induces pulmonary hypertension in mice by triggering T-cell dependent endothelial cell apoptosis
  • Circle diagram showing pregnancy-associated cardiac dysfunction and the role of RNAs
  • Diagram showing connecting sex-differences signaling, and microRNAs in cardiac fibrosis
  • Diagram showing the protective role of estrogen receptors in cardiovascular disease
  • Diagram showing role of oxidized lipids in pulmonary arterial hypertension

Two Postdoctoral Positions Available

NIH-funded postdoctoral positions are available in the laboratory of Dr Eghbali. The aim of the research is to elucidate molecular mechanisms of cardiovascular disease including pulmonary hypertension using molecular biology, biochemistry and pathophysiology related to heart dysfunction, pulmonary vascular biology, and animal models of heart and lung disease.

Candidates with a recent PhD degree in the field of cardiovascular disease, or pulmonary hypertension are encouraged to apply. Excellent written and verbal communication skills are required.

For more information, please contact Dr. Eghbali at meghbali@ucla.edu.