Elizabeta Nemeth
University of California-Los Angeles, CA·Physiology
Iron deficiency is one of the most common health problems in the world, with about 1.25 billion cases of iron deficiency anemia. Inflammation is also widespread.
- Fields
Physiology
Medicine & Clinical Research
Microbiology & Immunology
- Topics
iron deficiency
inflammation
sepsis
- Grants
- 1 known grant, through May 2028
What they work on
- Define how iron deficiency amplifies inflammation in a mouse model of sterile inflammation, examining macrophage behavior, the NF-κB inflammatory pathway and body-wide inflammatory signals.
- Determine how iron deficiency worsens acute lung injury triggered by LPS, a bacterial inflammatory molecule, and how it changes the role of the CREB transcription factor, a gene-controlling protein, in the lung.
- Determine how iron deficiency worsens LPS-induced acute kidney injury by modifying ER stress, a strain on the cell's protein-folding machinery, in kidney tissue.
More about the research
Often the two happen in the same person. This project asks whether lacking iron makes the body's inflammatory response more damaging to organs. That could matter in sepsis, a life-threatening reaction to infection, and possibly in other inflammatory diseases.
Why it matters
Iron deficiency is more common in disadvantaged groups, including low-income communities, Indigenous peoples and migrants from low- and middle-income countries. If iron deficiency worsens organ damage during inflammation, then managing iron better could help reduce lung and kidney injury in patients with sepsis or other inflammatory conditions. The findings could guide future clinical studies of this interaction in people.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Zhenjia Wang
University at Buffalo, NY·Biomedical Engineering
Engineer liposomes built from ionizable cationic lipids to deliver docosahexaenoic acid (DHA), an omega-3 fatty acid, into neutrophils and release it efficiently once inside.
Nicolae David
Northwestern University, IL·Physiology
Test whether inflammation suppresses HNF4α, a gene-activating transcription factor, in bone-forming osteoblasts, creating a feed-forward loop that blunts parathyroid hormone (PTH) response, by switching Hnf4α2 on or off in mice with CKD or PTH challenges.
Dean Sheppard
University of California-San Francisco, CA·Medicine & Clinical Research
Compare when inflammatory fibroblasts emerge, how long they persist and what they become in mouse lungs injured by bleomycin, silica or LPS, using Scube2-CreER lineage tracing of alveolar fibroblasts.
The school
University of California-Los Angeles: 84 labs on PI Pages, $1.9B a year on research, 803 research doctorates a year.
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