Awardee OrganizationWEILL MEDICAL COLL OF CORNELL UNIV
Description
Abstract Text
Project Summary/Abstract
Atrial fibrillation (AF) is the most common sustained arrhythmia with approximately one quarter of all
adults developing AF by the age of 80. AF can be symptomatic with people experiencing palpitations, racing
heart, syncope, congestive heart failure, and cardioembolic stroke. Epidemiologically, aging is associated
with AF and increasing obesity confers a stepwise higher lifetime risk of AF. Atrial myopathy and AF are thus
expected to become more rampant with the obesity and type 2 diabetes epidemics and the aging population.
The molecular mechanism(s) by which obesity leads to atrial fibrillation is poorly understood. We have
developed a new mouse model of spontaneous atrial fibrillation triggered by obesity. We found that
nicotinamide adenine dinucleotide (NAD+) and the Atf6 ER stress pathway are perturbed in obesity-induced
atrial fibrillation. Importantly, correcting NAD+ levels in the heart ameliorates atrial fibrillation. In this proposal,
we seek to follow up on these studies and assess the mechanisms by which NAD+ pathways protect against
atrial fibrillation. We will pursue the following specific aims: 1. Dissect the role of the NAD+ pathway in obesity-
induced AF. 2. Assess the role of the Atf6 ER stress pathway in obesity-induced AF. The overall goal of these
studies is to gain greater insight into the molecular pathogenesis of metabolic diseases and AF that may
ultimately lead to new treatments to prevent or ameliorate AF.
Public Health Relevance Statement
Public Health Relevance
Atrial fibrillation is an insidious disease with metabolic risk factors such as obesity, diabetes, and aging that
can range from asymptomatic to causing congestive heart failure and stroke. Despite our long-term
recognition of these risk factors, it is currently not known how the disease can be prevented in people with
obesity and diabetes. In this proposal, we aim to assess the mechanisms by which these metabolic risk factors
contribute to atrial fibrillation.
No Sub Projects information available for 1R01HL177651-01
Publications
Publications are associated with projects, but cannot be identified with any particular year of the project or fiscal year of funding. This is due to the continuous and cumulative nature of knowledge generation across the life of a project and the sometimes long and variable publishing timeline. Similarly, for multi-component projects, publications are associated with the parent core project and not with individual sub-projects.
No Publications available for 1R01HL177651-01
Patents
No Patents information available for 1R01HL177651-01
Outcomes
The Project Outcomes shown here are displayed verbatim as submitted by the Principal Investigator (PI) for this award. Any opinions, findings, and conclusions or recommendations expressed are those of the PI and do not necessarily reflect the views of the National Institutes of Health. NIH has not endorsed the content below.
No Outcomes available for 1R01HL177651-01
Clinical Studies
No Clinical Studies information available for 1R01HL177651-01
News and More
Related News Releases
No news release information available for 1R01HL177651-01
History
No Historical information available for 1R01HL177651-01
Similar Projects
No Similar Projects information available for 1R01HL177651-01