Yury Miller

About

Yury Miller is a Professor of Medicine at UC San Diego, with educational background from Russian State Medical University in Moscow, where he earned his MD in 1984 and PhD in 1990 in Biophysics. His research program focuses on the role of lipid metabolism and oxidation in fundamental biological processes and the development of human disease. His laboratory has made significant contributions by discovering the function of oxidized lipoproteins in activating toll-like receptors (TLRs), thereby connecting lipoprotein metabolism with inflammation in atherosclerosis. He pioneered the use of zebrafish models to study vascular lipid accumulation and inflammation, creating transgenic zebrafish lines with lipid abnormalities and genetic reporters for oxidized lipids. His work has led to discoveries regarding the functions of lipid and cholesterol metabolism in regulating vascular and neuroinflammation, neuropathic pain, and angiogenesis. Dr. Miller's research has been supported by multiple NIH grants, and he has contributed extensively to the understanding of immune mechanisms in atherosclerosis, neuroinflammation, and related fields.

Research topics

• Biology
• Medicine
• Chemistry
• Immunology
• Genetics
• Cell biology
• Endocrinology
• Virology
• Biochemistry
• Bioinformatics

Selected publications

• Lipid rafts as a therapeutic target

  Journal of Lipid Research · 2020 · 131 citations

  Senior authorCorresponding

  Lipid rafts regulate the initiation of cellular metabolic and signaling pathways by organizing the pathway components in ordered microdomains on the cell surface. Cellular responses regulated by lipid rafts range from physiological to pathological, and the success of a therapeutic approach targeting "pathological" lipid rafts depends on the ability of a remedial agent to recognize them and disrupt pathological lipid rafts without affecting normal raft-dependent cellular functions. In this articl…

  DOI

• Normalization of cholesterol metabolism in spinal microglia alleviates neuropathic pain

  The Journal of Experimental Medicine · 2021 · 101 citations

  Senior authorCorresponding

  Neuroinflammation is a major component in the transition to and perpetuation of neuropathic pain states. Spinal neuroinflammation involves activation of TLR4, localized to enlarged, cholesterol-enriched lipid rafts, designated here as inflammarafts. Conditional deletion of cholesterol transporters ABCA1 and ABCG1 in microglia, leading to inflammaraft formation, induced tactile allodynia in naive mice. The apoA-I binding protein (AIBP) facilitated cholesterol depletion from inflammarafts and reve…

  DOI

• Targeting Lipid Rafts—A Potential Therapy for COVID-19

  Frontiers in Immunology · 2020 · 60 citations

  COVID-19 is a global pandemic currently in an acute phase of rapid expansion. While public health measures remain the most effective protection strategy at this stage, when the peak passes, it will leave in its wake important health problems. Historically, very few viruses have ever been eradicated. Instead, the virus may persist in communities causing recurrent local outbreaks of the acute infection as well as several chronic diseases that may arise from the presence of a "suppressed" virus or…

  DOI

• AIBP protects retinal ganglion cells against neuroinflammation and mitochondrial dysfunction in glaucomatous neurodegeneration

  Redox Biology · 2020 · 52 citations

  mice had impaired visual function and Müller glia characterized by upregulated TLR4 activity, impaired mitochondrial network and function, increased oxidative stress and induced inflammatory responses. We also found that AIBP deficiency compromised mitochondrial network and function in RGCs and exacerbated RGC vulnerability to elevated IOP. Administration of recombinant AIBP prevented RGC death and inhibited inflammatory responses and cytokine production in Müller glia in vivo. These findings in…

  PublisherDOI

• AIBP: A New Safeguard against Glaucomatous Neuroinflammation

  Cells · 2024-01-21 · 15 citations

  reviewOpen access

  Glaucoma is a group of ocular diseases that cause irreversible blindness. It is characterized by multifactorial degeneration of the optic nerve axons and retinal ganglion cells (RGCs), resulting in the loss of vision. Major components of glaucoma pathogenesis include glia-driven neuroinflammation and impairment of mitochondrial dynamics and bioenergetics, leading to retinal neurodegeneration. In this review article, we summarize current evidence for the emerging role of apolipoprotein A-I bindin…

  PublisherOA PDFDOI

Recent grants

• NIH Grant R01HL124174

  NIH · $1.0M · 2019

• Reversal of preexisting neuropathic pain by spinal delivery of AIBP

  NIH · $377k · 2018–2022

• Role of TLR4-lipid rafts in nociception

  NIH · $2.3M · 2024–2028

Frequent coauthors

• Longhou Fang

  Houston Methodist

  105 shared

• John Y.‐J. Shyy

  University of California, San Diego

  65 shared

• Shing‐Jong Lin

  National Yang Ming Chiao Tung University

  64 shared

• Greg G. Geary

  Houston Methodist

  64 shared

• Shu Chien

  La Jolla Bioengineering Institute

  64 shared

• Po‐Hsun Huang

  Taipei Veterans General Hospital

  64 shared

• McKenna J. Geary

  University of California, San Diego

  64 shared

• Marcy Martin

  University of Zurich

  64 shared

Similar researchers at University of California, San Diego

• Michael (Geoff) Rosenfeldh-224
• Joseph Witztumh-181
• Alan Saltielh-112