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The research interests of Dr. Huo's laboratory are to study metabolic aspects of human
diseases in animal models.
These studies include examination of metabolic effect on leukocyte recruitment and
activation, fibroblast activation, activation and proliferation of vascular cells
in animal models of atherosclerosis, thrombosis, diabetes/obesity, pulmonary hypertension,
retinopathy, cardiac hypertrophy and renal fibrosis. The above diseases develop and
progress because of metabolic modulation in relevant cells. Dr. Huo's laboratory developed
in-vitro, ex-vivo, and in-vivo animal models and various engineered mice. Using these
animal disease models, epifluorescence intravital microscopy, FCAS and histological approaches as well as various molecular/genetic
assays, the phenotypes of disease models are characterized and the underlying molecular
mechanisms are studied. Current studies assess the involvement of AMPK, adenosine/adenosine
receptors, PFKFB3, ATIC and sirtuins in the development and progression of above diseases.
These studies are expected to augment basic understanding of metabolic aspect involved
in these diseases, and may lead to the development of metabolic therapy for future
clinical use in patients.
Adenosine receptor 2A in subretinal fibrosis
The propose of this project will test the hypothesis that adenosine receptor 2A (Adora2a)
mediated hypoxia inducible factor (Hif) signaling in choroidal endothelial cells (CECs)
and infiltrated macrophages enhance fibrotic effects leading to increased formation
of fibrotic lesions in choroidal neovascularization (CNV).
Myeloid PFKFB3 in Subretinal Fibrosis
The propose of this project will test the hypothesis that Pfkfb3-mediated glycolysis
in macrophages induces their transition to mesenchymal cells and/or myofibroblasts
and their production of profibrotic and proinflammatory factors by activating HIFs
pathways, eventually leading to subretinal fibrosis formation.
Targeting myeloid glycolysis in pathological ocular angiogenesis
The aims of this project are to investigate the role of PFKFB3 in myeloid cells in
retinal endothelial proliferation, migration as well as sprouting.
VSMC PFKFB3 in atherogenesis
This project is to study whether PFKFB3 deficiency in VSMCs inhibits VSMC proliferation,
migration and foam cell formation, ultimately reducing the formation of atherosclerotic
lesions in mice.
Mechanisms of myeloperoxidase and Nox4 interactions in abdominal aortic aneurysm
The purpose of this project is to determine how myeloperoxidase gets into the aortic
wall to cause aneurysms and explore whether medications that block white blood cells
from releasing myeloperoxidase can be used to treat aortic aneurysms.
AUGUSTA, Ga. (WJBF) – According to the CDC, heart disease is the leading cause of
death for men and women in the United States…and in the CSRA. Scientists at MCG have
discovered a new target in the treatment of the incurable disease. And regulating
that target could save hundreds of thousands of lives each year.
Coronary artery disease- the most common type of heart disease- occurs when cholesterol
and fat block the passage of blood flow to your heart.
Scientists at MCG have found that the smooth muscle cells that give those blood vessels
strength respond by getting bigger and multiplying. Unfortunately, this further contributes
to the disease.
Purine synthesis suppression reduces the development and progression of pulmonary
hypertension in rodent models. Eur Heart J. 2023 Jan 31:ehad044. doi: 10.1093/eurheartj/ehad044. Online ahead of
Single-cell transcriptome analyses reveal microglia types associated with proliferative
retinopathy. JCI Insight. 2022 Dec 8;7(23):e160940. doi: 10.1172/jci.insight.160940.PMID: 36264636
ATIC-Associated De Novo Purine Synthesis Is Critically Involved in Proliferative Arterial
Disease. Circulation. 2022 Nov 8;146(19):1444-1460. doi: 10.1161/CIRCULATIONAHA.121.058901.
Epub 2022 Sep 8.PMID: 36073366