Project Grant R01HL188552
- 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....
- 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 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 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 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 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 Child Health and Human Development awarded the University of Maryland, College Park $424,743 on June 25, 2026, under the Child Health and Human Development Extramural Research program (CFDA 93.865) to investigate the molecular basis of R249W LMNA-related congenital muscular dystrophy and explore therapeutic strategies. The research examines three specific aims: characterizing how the R249W mutation affects skeletal muscle development; studying lamina organization and...
- The National Heart, Lung, and Blood Institute (NHLBI), part of the Department of Health and Human Services National Institutes of Health, awarded The Medical College of Wisconsin, Inc. $792,011 on July 15, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837) to validate plasma cell-free DNA (CFDNA)—including nuclear and mitochondrial variants—as a clinically actionable biomarker for predicting critical post-surgical events in infants undergoing complex congenital heart surgery....
- The National Institute of General Medical Sciences awarded the Carnegie Institution of Washington $335,000 on September 9, 2025, under the Biomedical Research and Research Training program (CFDA 93.859) to investigate how lamins regulate three-dimensional genome organization and gene expression during development. The project will characterize the mechanisms by which lamin proteins control nuclear lamina-associated domains and chromatin architecture in mouse embryonic stem cells and embryonic...
- The National Heart, Lung, and Blood Institute, part of the National Institutes of Health under the Department of Health and Human Services, awarded The Medical College of Wisconsin, Inc., $234,000 on July 1, 2026, under the Cardiovascular Diseases Research program (CFDA 93.837). The Medical College of Wisconsin will conduct a single-cell dissection of cellular and transcriptional dynamics driving post-transplant relapse in myelodysplastic syndromes (MDS). The research leverages longitudinal...
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 arrhythmic storms, transplant, death, or major cardiac events by age 45. The funded research addresses cellular heterogeneity across LMNA mutations by characterizing a library of 178 LMNA mutations associated with skeletal muscular dystrophy, cardiac disease, premature aging, and lipodystrophy. The study identified that approximately 48 percent of LMNA-ACM mutations do not form protein aggregates and lack significant misfolding, despite aggregation in most myopathic variants. Multiomic investigation revealed divergent cellular pathways: aggregating variants demonstrate abnormal scaffolding and metabolic perturbations, while non-aggregating mutations show dominant changes in DNA/RNA damage and protein homeostasis. The research hypothesizes that cardiomyocytes' continuous mechanical load shapes these divergent phenotypes, and seeks to identify mutation-specific therapeutic targets. Performance occurs in Madison, Wisconsin, with a period of performance ending April 30, 2030.
Mod # | Description | ReasonForModification | Federal Obligation | Date |
|---|---|---|---|---|
| Not listed | $789.6k | 8/19/26 |