# FKBP5 AND CARDIAC ARRHYTHMOGENESIS

> **NIH NIH R01** · BAYLOR COLLEGE OF MEDICINE · 2024 · $40,845

## Abstract

PROJECT SUMMARY
Atrial fibrillation (AF) is the most frequent arrhythmia. AF is uniquely associated with the development of heart
failure with preserved ejection fraction (HFpEF). Both AF and HFpEF are associated with metabolic syndromes.
Cardiac remodeling during HFpEF can be partially explained by changes in substrate utilization, AKT signaling,
and enhanced insulin resistance. As a chaperon protein, FKBP5 is known to modulate the phosphorylation and
activity of AKT via PHLPP. Mice that lack FKBP51 exhibited increased AKT activity and increased insulin
resistance. The role of ‘FKBP5 – PHLPP – AKT’ signaling in the concomitant AF and HFpEF has not been
reported previously. We recently have reported that the loss of FKBP5 can lead to cardiac fibrosis, atrial
myopathy, and enhanced AF inducibility. Whether the increased AF susceptibility, due to the loss of FKBP5, can
perpetuate the progression of HFpEF remains an open question. In this application, we will test the hypothesis
that FKBP5 deficiency accelerates the progression of HFpEF by promoting the development of AF.

## Key facts

- **NIH application ID:** 11063683
- **Project number:** 3R01HL164838-01A1S1
- **Recipient organization:** BAYLOR COLLEGE OF MEDICINE
- **Principal Investigator:** Na Li
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2024
- **Award amount:** $40,845
- **Award type:** 3
- **Project period:** 2024-08-01 → 2026-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/11063683

## Citation

> US National Institutes of Health, RePORTER application 11063683, FKBP5 AND CARDIAC ARRHYTHMOGENESIS (3R01HL164838-01A1S1). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/11063683. Licensed CC0.

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