Chiara Giannarelli
New York University, NY·Medicine & Clinical Research
Atherosclerosis is the buildup of fatty, inflamed plaques in artery walls. It underlies most heart attacks and strokes.
- Fields
Medicine & Clinical Research
Microbiology & Immunology
Physiology
- Topics
atherosclerosis
atherosclerotic cardiovascular disease
plaque inflammation
- Grants
- 2 known grants, through Feb 2028
What they work on
- Determine how cytotoxic γδ T cells contribute to atherosclerosis progression in type 2 diabetes, and whether the transcription factor ZEB2 drives their harmful functions, using mouse models and human plaque data.
- Identify how γδ T cells and ZEB2 impair plaque regression after lipid lowering in a mouse model of type 2 diabetes and atherosclerosis.
- Define the role of neuropilin-1 (NRP1), an alternative SARS-CoV-2 entry receptor on plaque macrophages, in virus-induced plaque inflammation and atherosclerosis progression.
- Determine how persistent non-infectious SARS-CoV-2 RNA debris drives inflammation and plaque growth after viral clearance, using human vascular explants and the Syrian golden hamster model.
More about the research
Some conditions make it much worse, and standard treatments often fail to fully protect these patients. Both projects ask how immune activity inside human plaques drives that extra risk: one in type 2 diabetes, the other after SARS-CoV-2 (COVID-19) infection. Each combines human plaque tissue, single-cell analysis and animal models.
Why it matters
Type 2 diabetes, projected to affect more than 600 million people, and COVID-19 both raise the risk of heart attack and stroke beyond what current treatments control. Finding immune drivers such as γδ T cells, ZEB2 and the viral entry receptor NRP1 could point to new therapy targets for lowering cardiovascular risk in these patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Karin Bornfeldt
University of Washington, WA·Medicine & Clinical Research
Test whether higher plasma APOC3, a protein that controls triglyceride-rich particles, tracks with build-up of a mid-sized lipoprotein particle and worsening insulin resistance and arterial stiffness in youth with type 1 or type 2 diabetes followed over time.
Daniel Li
Stanford University, CA·Genetics·Early-career
Determine how losing ZEB1, a transcription factor linked to coronary artery disease risk, changes gene activity, epigenetic state and plaque features in smooth muscle–derived cells, using a Zeb1 knockout mouse model of atherosclerosis.
Guizhen Zhao
University of Houston, TX·Physiology
Define whether the BAF60c–PPARγ axis protects against atherosclerosis, using male and female mice with smooth-muscle-specific knockout or transgenic overexpression of BAF60c, a chromatin-remodeling subunit.
The school
New York University: 72 labs on PI Pages, $1.5B a year on research, 540 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.