Neural control of heart regenerative potential
Description: Smoking is a primary cause of heart disease and accounts for thirty percent of all deaths from cardiovascular diseases in the United States. Tobacco smoke contains high levels of carbon monoxide and nicotine. Due to reduced blood oxygenation by carbon monoxide and increased heart rate and blood pressure by nicotine, cigarette smokers are more susceptible to heart attacks, characterized by coronary artery blockade, myocyte death and replacement fibrosis, ultimately leading to possible fatal arrhythmia and heart failure. Unfortunately, cardiomyocyte (CM) loss in adult humans is irreversible. Recent studies show the promise of inducing CM proliferation for cardiac regeneration to treat patients following myocardial infarction.
Neonatal mice exhibit a robust heart regenerative capability which quickly diminish one week after birth as CMs permanently withdraw from the cell cycle. Recently, we identified thyroid hormone signaling as a major driver of CM cell-cycle exit and regenerative potential loss. In this proposal, we plan to study how the peripheral nerve system regulates CM renewal in postnatal growth and heart injury repair, and how this process is influenced by thyroid hormones and nicotine. Altogether, our work will advance our understanding on why our heart can’t regenerate and how tobacco smoking may impact heart repair.
Amount: $1,170,000
Funding type: grant
Funder scheme: High Impact Research Project
Start date: 2022-07-01
End date: 2026-06-30
Investigator: Guo Huang
Institution: UCSF
Funded outputs count: 0
Funder award ID: T32IR4826
OpenAlex ID: G2361007328