R01HL170249
Project Grant
Overview
Grant Description
Inflammation-resolution impairments in aging and atherosclerosis - Summary
Aging is a major risk factor for atherosclerotic cardiovascular disease (CVD) and yet mechanisms as to how aging impacts this disease remains vastly underexplored. Aging is associated with non-resolving inflammation (inflammaging). The resolution of inflammation requires the balance between pro-inflammatory leukotrienes (LTS, e.g. LTB4) or prostaglandins (PGs) and W3-derived specialized pro-resolving mediators (SPMs), like resolvins.
While it is now known that atherosclerosis is associated with a reduced SPM:LT or PG mediator ratio, major gaps exist in our understanding of (a) the mechanisms regulating impaired resolution in age-related atherosclerosis and (b) how SPMs promote resolution. Our objective is to investigate mechanisms of defective resolution in aging so that we can develop novel strategies to treat atherosclerosis in the physiological context of aging.
We found a new link in which aged atherosclerotic mice had impaired resolution of atherosclerosis, exhibited exuberant granulopoiesis and defective SPM signaling in the bone marrow. We propose three highly integrated, but independent, aims to address mechanisms regulating myelopoiesis in aging and atherosclerosis and to determine the efficacy and mechanisms of resolvin therapies in aging and atherosclerosis.
These aims will address a fundamental gap in our understanding of the physiologically relevant context of aging in atherosclerosis. Completion of the proposed studies will provide mechanistic insight into dysregulated resolution processes in aging, define cells, mediators, and mechanisms restraining plaque resolution/regression in aging, and establish rationales for new therapies.
Aging is a major risk factor for atherosclerotic cardiovascular disease (CVD) and yet mechanisms as to how aging impacts this disease remains vastly underexplored. Aging is associated with non-resolving inflammation (inflammaging). The resolution of inflammation requires the balance between pro-inflammatory leukotrienes (LTS, e.g. LTB4) or prostaglandins (PGs) and W3-derived specialized pro-resolving mediators (SPMs), like resolvins.
While it is now known that atherosclerosis is associated with a reduced SPM:LT or PG mediator ratio, major gaps exist in our understanding of (a) the mechanisms regulating impaired resolution in age-related atherosclerosis and (b) how SPMs promote resolution. Our objective is to investigate mechanisms of defective resolution in aging so that we can develop novel strategies to treat atherosclerosis in the physiological context of aging.
We found a new link in which aged atherosclerotic mice had impaired resolution of atherosclerosis, exhibited exuberant granulopoiesis and defective SPM signaling in the bone marrow. We propose three highly integrated, but independent, aims to address mechanisms regulating myelopoiesis in aging and atherosclerosis and to determine the efficacy and mechanisms of resolvin therapies in aging and atherosclerosis.
These aims will address a fundamental gap in our understanding of the physiologically relevant context of aging in atherosclerosis. Completion of the proposed studies will provide mechanistic insight into dysregulated resolution processes in aging, define cells, mediators, and mechanisms restraining plaque resolution/regression in aging, and establish rationales for new therapies.
Awardee
Funding Goals
NOT APPLICABLE
Grant Program (CFDA)
Awarding / Funding Agency
Place of Performance
Albany,
New York
122083412
United States
Geographic Scope
Single Zip Code
Related Opportunity
Analysis Notes
Amendment Since initial award the total obligations have increased 294% from $802,138 to $3,156,451.
Albany Medical College was awarded
Age-Related Atherosclerosis: Investigating Resolution Mechanisms
Project Grant R01HL170249
worth $3,156,451
from National Heart Lung and Blood Institute in June 2023 with work to be completed primarily in Albany New York United States.
The grant
has a duration of 4 years and
was awarded through assistance program 93.837 Cardiovascular Diseases Research.
The Project Grant was awarded through grant opportunity NIH Research Project Grant (Parent R01 Clinical Trial Not Allowed).
Status
(Ongoing)
Last Modified 6/5/26
Period of Performance
6/1/23
Start Date
5/31/27
End Date
Funding Split
$3.2M
Federal Obligation
$0.0
Non-Federal Obligation
$3.2M
Total Obligated
Activity Timeline
Transaction History
Modifications to R01HL170249
Additional Detail
Award ID FAIN
R01HL170249
SAI Number
R01HL170249-3905906072
Award ID URI
SAI UNAVAILABLE
Awardee Classifications
Private Institution Of Higher Education
Awarding Office
75NH00 NIH National Heart, Lung, and Blood Institute
Funding Office
75NH00 NIH National Heart, Lung, and Blood Institute
Awardee UEI
G6VVMPNK4Y48
Awardee CAGE
6D762
Performance District
NY-20
Senators
Kirsten Gillibrand
Charles Schumer
Charles Schumer
Budget Funding
| Federal Account | Budget Subfunction | Object Class | Total | Percentage |
|---|---|---|---|---|
| National Heart, Lung, and Blood Institute, National Institutes of Health, Health and Human Services (075-0872) | Health research and training | Grants, subsidies, and contributions (41.0) | $802,138 | 100% |
Modified: 6/5/26