Deepa Sathyaseelan
University of Oklahoma-Health Sciences Center, OK·Physiology
As people age, low-level inflammation builds up throughout the body. This 'inflammaging' is linked to many diseases of old age.
- Fields
Physiology
Microbiology & Immunology
Neuroscience
- Topics
aging
necroptosis
hepatocytes
- Grants
- 1 known grant, through Jun 2029
What they work on
- Determine whether necroptosis in hepatocytes, a cell death that spills inflammatory molecules like HMGB1, activates liver macrophages and drives liver inflammation, using mice in which necroptosis is turned on or off in hepatocytes.
- Test whether hepatocyte necroptosis increases cellular senescence and causes liver damage such as fat build-up and scarring, using mouse models with hepatocyte-specific changes in necroptosis.
- Determine whether hepatocyte necroptosis raises circulating HMGB1 and causes brain inflammation, glial cell activation and behavioral deficits in mice.
More about the research
In the liver, it accompanies chronic liver disease, a leading cause of liver transplants and death in older adults. Liver inflammation is also thought to contribute to brain inflammation and memory and thinking problems. However, no one knows what drives liver inflammation with age, or how it reaches the brain.
Why it matters
Chronic liver disease and cognitive decline are common in older adults. Showing that dying liver cells drive both liver damage and brain inflammation could reveal new targets. Blocking necroptosis in hepatocytes might one day help reduce age-related liver disease and memory and thinking problems.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Xiaoqin Wu
University of Texas Health Science Center at Houston, TX·Microbiology & Immunology·Early-career
Characterize liver immune cell populations and cell death after Gao-binge alcohol feeding in Mlkl bone-marrow chimeric mice, using flow cytometry of isolated non-parenchymal liver cells.
Hongxue Shi
Louisiana State University Health Sciences Center-Shreveport, LA·Medicine & Clinical Research·Early-career
Test whether loss of TIM4, a macrophage receptor that captures apoptotic cells, impairs clearance of dying liver cells and speeds NASH fibrosis, by deleting or restoring macrophage TIM4 in NASH mice.
Xiaohong Lu
Louisiana State University Health Sciences Center-Shreveport, LA·Neuroscience
Determine whether SARS-CoV-2 infection drives chronic loss of smell and cognitive deficits in humanized ACE2 transgenic mice, in a model that produces lasting brain pathology without the virus invading the brain.
The school
University of Oklahoma-Health Sciences Center: 11 labs on PI Pages, $474M a year on research, 31 research doctorates a year.
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