# Transcriptomic and epigenetic regulators of Drosophila heart aging

> **NIH NIH R21** · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · 2020 · $243,750

## Abstract

SUMMARY
In the United Sates, heart disease is the leading cause of death for men and women, killing about 610,000 people
each year. The incidence of heart failure approximately doubles through each decade of life. Consequently, due
to ongoing aging of human populations across the globe, heart disease and associated morbidity and mortality
is expected to become an even greater social and economic burden. This trend will be exacerbated by the
increasing incidence of obesity. The aging heart shows many and diverse changes with age, typically
detrimental. These include structural changes, functional changes, impaired repair and increased cardiovascular
disease. Evidence already indicates that age-associated changes to the epigenome and transcriptome contribute
to pathologies of the aging heart. Importantly, the epigenome is maintained in a state of dynamic equilibrium and
is prone to “drift” over the lifespan. Accordingly, we hypothesize that homeostasis of the dynamic chromatin
steady state (a process we have termed “chromostasis”) of heart cardiomyocytes is critical for maintenance of
an appropriate gene expression program and phenotype, and function at the cellular and tissue levels, over the
life span. However, eventually, age-associated drift of the epigenome is likely to promote age-associated
changes to the transcriptome and cell phenotype and so increased heterogeneity within aged tissues. We
anticipate that this heterogeneity in old hearts is manifest at several levels: between cardiomyocytes isolated
from normal and poor functioning whole aged hearts (in a population of aged flies, there is fly-to-fly variation in
heart function); and between sub-regions of normal and impaired function within a single aged heart (in a single
heart, there are regions of normal and impaired function). We hypothesize that age-associated epigenetic and
transcriptomic alteration and tissue heterogeneity contribute to dysfunction of the aged heart. We further
hypothesize that specific epigenetic regulators are required for homeostasis of the heart epigenome and
transcriptome, and thereby promote healthy aging and longevity.
Specific Aim 1. Investigate age-associated transcriptomic alteration and heart heterogeneity and
correlate with heart dysfunction.
Specific Aim 2. Identify additional epigenetic regulators that influence healthy aging of the heart.

## Key facts

- **NIH application ID:** 9999384
- **Project number:** 5R21AG058075-02
- **Recipient organization:** SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE
- **Principal Investigator:** PETER D. ADAMS
- **Activity code:** R21 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2020
- **Award amount:** $243,750
- **Award type:** 5
- **Project period:** 2019-09-01 → 2021-05-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/9999384

## Citation

> US National Institutes of Health, RePORTER application 9999384, Transcriptomic and epigenetic regulators of Drosophila heart aging (5R21AG058075-02). Retrieved via AI Analytics 2026-05-22 from https://api.ai-analytics.org/grant/nih/9999384. Licensed CC0.

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