Project Grant R01HL183935
- The National Heart, Lung, and Blood Institute awarded $108,656 to the University of Wisconsin–Madison on March 3, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to characterize the molecular mechanisms of phospholamban R14DEL cardiomyopathy. The recipient will use high-resolution mass spectrometry–based proteomics, human clinical samples, and patient-specific human induced pluripotent stem cell–derived cardiomyocytes to investigate how cardiac proteoform alterations drive...
- The National Heart, Lung, and Blood Institute awarded Cedars-Sinai Medical Center $1.481 million on July 6, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate single-cell proteome heterogeneity arising from myosin heavy chain 7 (MYH7) mutations associated with hypertrophic cardiomyopathy and the recovery mechanisms induced by the therapeutic agent mavacamten. The research applies high-sensitivity mass spectrometry and single-cell proteomics to quantify over...
- The National Heart, Lung, and Blood Institute awarded the University of Wisconsin - Madison $1.211 million on September 15, 2025, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate neutral sphingomyelinase (NSMASE) in cardiac mechanosensing and mechanical regulation of the heart. The project addresses NSMASE as a critical membrane enzyme involved in sphingolipid metabolism that regulates both normal physiological heart function in response to acute changes in cardiac...
- The National Heart, Lung, and Blood Institute awarded the University of Wisconsin - Madison $789,648 in funding under the Cardiovascular Diseases Research program (CFDA 93.837) on August 17, 2026, for research resolving mutation-specific early disease features of LMNA variants to identify therapeutic targets in arrhythmogenic cardiomyopathy (ACM). LMNA encodes lamin A/C, and mutations can cause ACM, a condition currently lacking disease-modifying medications. LMNA-ACM patients face risk of...
- The National Heart, Lung, and Blood Institute awarded the University of Wisconsin - Madison $747,262 on June 1, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to define the multi-omics landscape of phospholamban-induced cardiomyopathy for precision medicine. The research applies top-down proteomics to study post-translational modifications, genetic variants, and splicing isoforms in phospholamban (PLN) gene variants, specifically the PLN-R14DEL deletion associated with...
- The National Heart, Lung, and Blood Institute (NHLBI) awarded the University of Washington $2,647,494 on May 1, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to develop computational and experimental models of myosin variants that determine how single amino acid variants affect myosin structure and function across multiple scales. The project integrates molecular and Brownian dynamics simulations of the chemo-mechanical cycle of β-myosin, generated from human crystal and...
- The National Heart, Lung, and Blood Institute awarded the University of Wisconsin–Madison $151,040 on February 5, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate the assembly and localization of HERG channel cotranslational complexes in cardiac tissue. The research examines how heart cells co-regulate functionally related ion channels at the translational level during protein biosynthesis, with focus on HERG1A and HERG1B channel assembly. The project uses...
- The National Institute of General Medical Sciences awarded The Leland Stanford Junior University $494,796 on March 1, 2026, to investigate myosin structure and function in hereditary cardiac disease, specifically familial hypertrophic cardiomyopathy (HCM). The award funds research into how mutations in cardiac myosin and myosin binding protein C—which account for approximately 90 percent of HCM cases—disrupt the biochemical and biomechanical function of the myosin motor, leading to cardiac...
- The National Heart, Lung, and Blood Institute awarded Masonic Medical Research Institute $775,089 on August 1, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate transcriptional regulation in hypoplastic left heart syndrome. The research examines the role of MYRF, a transcription factor linked to HLHS, a congenital heart disease characterized by a small left ventricular chamber, thick left ventricular wall, and negligible left ventricular function. The work...
- The National Institutes of Health National Heart, Lung, and Blood Institute awarded the University of Arizona $650,419 on July 15, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate how myosin and cardiac thin filament mutations cause allosteric dysfunction in hypertrophic cardiomyopathy. The research extends a program studying sarcomere function in health and disease. The project develops coupled time-resolved FRET computation-based methods to characterize...
The National Heart, Lung, and Blood Institute awarded the University of Wisconsin - Madison $581,307 on September 1, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to investigate mutation-specific responses to myosin inhibitors in human iPSC models of hypertrophic cardiomyopathy. The research evaluates how different HCM-causing mutations in genes encoding cardiac sarcomeric proteins respond to mavacamten, a myosin ATPase inhibitor approved to treat obstructive HCM. Mavacamten reduces left ventricular hypertrophy and improves exercise capacity in many patients, but failed to benefit approximately 30 percent of obstructive HCM patients and produced no symptomatic improvement in non-obstructive HCM. The project applies a validated human stem cell-derived engineered heart tissue platform using six isogenic iPSC lines, each expressing a known HCM-causing mutation, to characterize functional differences between responder and non-responder mutations. The work hypothesizes that individual mutations produce distinct biophysical effects on myosin cross-bridge dynamics—specifically, differential changes in the disordered relaxed and super-relaxed states of myosin—that may explain heterogeneous therapeutic responses to mavacamten. Work is performed in Madison, Wisconsin. The period of performance runs from September 1, 2026, through May 31, 2030. The assistance type is a project grant.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $581.3k | 9/1/26 |