# NIH grant: The Pyruvate-Lactate Metabolic Axis in Heart Failure and Recovery (1R01HL180922-01A1) — retained record

> Retained us-gov-api record from us-gov-api:nih-reporter.

Canonical: https://highsignal.app/data/records/a93fb13dcfb1047f

[← sources](https://highsignal.app/data)


source: [us-gov-api](https://highsignal.app/data/us-gov-api) (us-gov-api:nih-reporter)  published 2026-06-20 00:00 ingested 2026-06-28 12:46

[original source ↗](https://reporter.nih.gov/project-details/1R01HL180922-01A1)

## retained text



```
NIH grant 1R01HL180922-01A1: The Pyruvate-Lactate Metabolic Axis in Heart Failure and Recovery
Institute: {'code': 'HL', 'abbreviation': 'NHLBI', 'name': 'National Heart Lung and Blood Institute', 'admin_org_id': '12500068', 'admin_funding_url': ''}. PI: Stavros George Drakos. Award: $635681.
Start: 2026-06-20T00:00:00.
PROJECT SUMMARY/ABSTRACT
Heart failure (HF) is a leading cause of mortality worldwide. The metabolism of the failing heart is commonly
characterized by increased glucose uptake, glycolytic dependence, and reduced oxidative phosphorylation. We
previously demonstrated that blocking glucose oxidation is sufficient to cause hypertrophy and subsequent HF.
Additionally, our preliminary data shows that an altered pyruvate-lactate metabolic axis may be pivotal in human
HF. Research investigating both the mechanistic regulation and biological roles of the pyruvate-lactate metabolic
axis in cardiac metabolism during HF and cardiac recovery is warranted and also has the potential to identify
novel druggable pathways to target for future pharmacological approaches.
The overall objective of this application is to test the hypothesis that impaired pyruvate oxidation is a
cardinal feature of HF in humans and animal models and that myocardial recovery is tightly coupled to
normalization of the pyruvate-lactate metabolic axis. We will quantify the pyruvate-lactate metabolic axis in
human HF and myocardial recovery (Aim 1). Next, we will determine the essentiality of the pyruvate-lactate
metabolic axis for HF and cardiac recovery (Aim 2). Lastly, we will define cell-autonomous mechanisms that
regulate the pyruvate-lactate axis in HF and recovery (Aim 3). These experiments will allow us to identify patterns
of metabolic alteration in the pyruvate-lactate axis and molecular pathways during HF and myocardial recovery.
Understanding the role of pyruvate and lactate metabolism in HF and myocardial recovery is cutting-edge
research. Our unique access to human HF myocardium from patients administered stable isotope-labeled
glucose or lactate to quantitate pyruvate metabolism in HF and recovery is state-of-the-art and will likely
help us reveal new fundamental mechanisms of cardiac metabolism and expedite the successful translation of
therapeutics being validated in various models of HF and recovery.
```



document fetched 2026-06-28 13:47