Official websites use .gov

A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS

A lock ( 🔒 ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

Need Help

The Role of the Endothelial Circadian Clock in Doxorubicin-Induced Cardiotoxicity

Award Number: F31HL189138
ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS
PERIOD OF PERFORMANCE START DATE: 02/06/2027
PERIOD OF PERFORMANCE END DATE: 02/05/2028

Group Awards By:

View Award Description

The Role of the Endothelial Circadian Clock in Doxorubicin-Induced Cardiotoxicity - ABSTRACT Cardiovascular disease (CVD) is a leading cause of morbidity and mortality among cancer survivors, particularly those treated with anthracyclines such as doxorubicin (DOXO), which are known to induce long-term cardiotoxic effects including endothelial dysfunction, cardiomyopathy, and heart failure. Despite the widespread use of anthracyclines in pediatric and adult oncology, current strategies to prevent chemotherapy-induced cardiovascular toxicity remain limited, and the underlying mechanisms are poorly understood. Evidence implicates the circadian clock—a critical regulator of physiological rhythms—in cardiovascular health, with deregulation linked to endothelial dysfunction and CVD. However, its role in chemotherapy-induced cardiac injury, particularly through effects on endothelial cells—which are essential for maintaining vascular health—has not been fully elucidated. Preliminary data from our laboratory demonstrate that DOXO exposure disrupts circadian clock expression in human coronary artery endothelial cells, with dose-dependent alterations in core clock components such as BMAL1, CLOCK, PER1/2, and CRY2, correlating with markers of endothelial activation, cell cycle arrest, and apoptosis. These findings suggest that circadian clock disruption may be a key contributor to DOXO-induced endothelial toxicity. The proposed research will investigate the central hypothesis that endothelial circadian clock components are essential for maintaining cardiovascular homeostasis under chemotherapeutic stress. Aim 1 will determine the relevance of the circadian clock in endothelial injury response to doxorubicin exposure. Aim 2 will define the impact of endothelial Bmal1 deficiency on cardiovascular homeostasis in response to doxorubicin induced cardiotoxicity. Completion of these studies will provide foundational insights into the molecular mechanisms of chemotherapy-induced cardiovascular toxicity and identify novel targets for cardioprotection ultimately advancing strategies for promoting cardiovascular health in cancer survivors.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2026 ( Subtotal = $39,985 )
2026	2026	FLORIDA ATLANTIC UNIVERSITY	777 GLADES RD	BOCA RATON	FL	33431	PALM BEACH	USA	Cardiovascular Diseases Research	000	1	8/11/2026	NEW	$39,985
														Subtotal = $39,985

Grand Total All Awards = $39,985

Top

All Categories

About

Search

Reports

Data Submission

Award Information

The Role of the Endothelial Circadian Clock in Doxorubicin-Induced Cardiotoxicity

Award Number: F31HL189138

ORGANIZATION: NATIONAL HEART, LUNG, & BLOOD INSTITUTE

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: FELLOWSHIP/SCHOLARSHIP/STUDENT LOANS

PERIOD OF PERFORMANCE START DATE: 02/06/2027

PERIOD OF PERFORMANCE END DATE: 02/05/2028

Federal Websites

Department of Health & Human Services

HHS Operating Divisions

HHS Staff Divisions

Download A Document Viewer