# The epigenetic regulation of inflammation in tissue repair and vascular disease

> **NIH NIH R35** · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2024 · $1,053,460

## Abstract

PROJECT SUMMARY
The overarching theme for our research program over the past 10 years has been to better understand the
etiology and pathogenesis of chronic inflammation in tissue repair processes and vascular disease, with a
particular interest in how epigenetics influences the innate immune response and shapes pathologic and
homeostatic processes. Our laboratory has contributed seminal studies related to 1) epigenetic regulation of
myeloid cells that alter inflammation in abdominal aortic aneurysms (AAA), 2) regulation of macrophage
phenotypes by chromatin modifying enzymes (CMEs) during tissue repair, 3) prostaglandin regulation of
macrophage plasticity in the setting of tissue repair, 4) chemokines and other signaling pathways driving
monocyte recruitment to injured tissue and tissue macrophage phenotypes, 5) epigenetic alterations that
impact macrophage function in COVID-19 infection, 6) metabolomic and other biomarker studies in tissue
regeneration and cardiovascular disease, 7) role of epigenetic regulation of macrophages following recovery
from sepsis. Our work has utilized animal models to carry out mechanistic studies and patient-derived cells and
tissues to confirm relevant pathways, identify therapeutic targets and characterize novel biomarkers. Based on
our previously published observations and novel preliminary data, our laboratory is broadly focused in 4 main
areas. The first serves as a continuation and expansion of HL156274 grant (currently in year 2) to complete
and advance therapeutically relevant studies of JMJD3 and other critical CMEs in AAA development. The
second goal will serve as renewal of HL137919 and allow us explore JAK/STAT signaling in tissue
macrophages and blood monocytes and the downstream regulation of CMEs and subsequent inflammation in
a variety of conditions (tissue regeneration, AAAs and post-sepsis recovery). The third goal will be to explore
the interactions between structural cells (SMCs, keratinocytes, fibroblasts) and myeloid cells in the setting of
tissue regeneration and AAA development. The fourth will be an expansion into the area of peripheral
atherosclerosis where we will explore epigenetic regulation of macrophage phenotype/function in the setting of
peripheral atherosclerotic disease (PAD). This emerging investigator award (EIA) mechanism will allow us to
extend our studies in each of these areas and will allow for mechanistic understanding of the role of epigenetic
regulation of macrophage phenotypes in the pathogenesis of a breadth of cardiovascular disease processes
including tissue regeneration, aneurysm formation and peripheral atherosclerosis. It will also allow our
laboratory to complete proof-of-concept and validation studies needed in both animals and humans to advance
new therapies to the clinics for treatment of cardiovascular diseases.

## Key facts

- **NIH application ID:** 10843045
- **Project number:** 5R35HL167143-02
- **Recipient organization:** UNIVERSITY OF MICHIGAN AT ANN ARBOR
- **Principal Investigator:** Katherine Ann Gallagher
- **Activity code:** R35 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $1,053,460
- **Award type:** 5
- **Project period:** 2023-07-01 → 2030-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10843045

## Citation

> US National Institutes of Health, RePORTER application 10843045, The epigenetic regulation of inflammation in tissue repair and vascular disease (5R35HL167143-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/10843045. Licensed CC0.

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