Pinet, Florence
Mayo Clinic
Inserm U1167, Institut Pasteur de Lille, Université de Lille, Lille, France.
Citations 2
Novel association of NAV3 with dilated cardiomyopathy and its role in cardiac fibrosis
wang, Min, Ghazal, Rachad , Srinivas, Akshatha N. , Nguyen, Thanh Thanh L. , Murthy, Vishakantha , McNamara, D., Skime, Michelle , Batzler, Anthony , Jenkins, Gregory D. , Barlera, Simona, Mestroni, Luisa, Merlo, Marco, Pinet, Florence, Krejčí, Jan, Chaloupka, Anna , Groote, Pascal. De, Weinshilboum, RM, Tschumperlin, Daniel J. , Liu, Duan , Pereira, Naveen, McNamara, Dennis M. , Nguyen, Thanh Thanh L. , Wang, Min , Ghazal, Rachad , Wang, Min , McNamara, Dennis M , Skime, Michelle K , Pileggi, Silvana , Mestroni, Luisa , Pinet, Florence , Krejčí, Jan , Chaloupka, Anna , de Groote, Pascal , Weinshilboum, Richard M. , Tschumperlin, Daniel J , Liu, Duan , Pereira, Naveen L , Pileggi, Silvana , Mestroni, Luisa , Merlo, Marco , Pinet, F , Krejčí, Jan , Groote, Pascal de
American Journal of Physiology-Heart and Circulatory Physiology | January 29, 2026 | Volume: 330 | Issue: 3 | Pages: H686-H696
This study uncovers a previously unrecognized role for NAV3 in TGF-β1-driven cardiac fibroblast activation. We show that NAV3 facilitates profibrotic remodeling through noncanonical signaling and cell cycle arrest, independently of SMAD2/3. These findings position NAV3 as a novel regulator of fibroblast phenotype and a potential modulator of cardiac fibrosis.
Myocardial Recovery in Recent Onset Dilated Cardiomyopathy: Role of CDCP1 and Cardiac Fibrosis
Liu, Duan , Wang, Min , Murthy, Vishakantha , McNamara, Dennis M. , Nguyen, Thanh Thanh L. , Philips, Trudy Janice , Vyas, Hridyanshu , Gao, Huanyao , Sahni, Jyotan , Starling, Randall C. , Skime, Michelle , Batzler, Anthony , Jenkins, Gregory D. , Barlera, Simona, Pileggi, Silvana , Mestroni, Luisa , Merlo, Marco , Pinet, F , Krejčí, Jan , Chaloupka, Anna , Groote, Pascal de , Tschumperlin, Daniel J. , Weinshilboum, Richard M. , Pereira, Naveen L. , Philips, Trudy J, Cooper, Leslie T , Skime, Michelle K , Batzler, Anthony , Pileggi, Silvana , Mestroni, Luisa , Sinagra, Gianfranco , Pinet, Florence , Krejčí, Jan , Chaloupka, Anna , Miller, Jordan D. , de Groote, Pascal , Pereira, Naveen L , Nguyen, Thanh Thanh L. , Wang, Min , Liu, Duan , Cooper, Leslie T. , Weinshilboum, Richard M.
Circulation Research | October 6, 2023 | Volume: 133 | Issue: 10 | Pages: 810-825
BACKGROUND: Dilated cardiomyopathy (DCM) is a major cause of heart failure and carries a high mortality rate. Myocardial recovery in DCM-related heart failure patients is highly variable, with some patients having little or no response to standard drug therapy. A genome-wide association study may agnostically identify biomarkers and provide novel insight into the biology of myocardial recovery in DCM. METHODS: A genome-wide association study for change in left ventricular ejection fraction was performed in 686 White subjects with recent-onset DCM who received standard pharmacotherapy. Genome-wide association study signals were subsequently functionally validated and studied in relevant cellular models to understand molecular mechanisms that may have contributed to the change in left ventricular ejection fraction. RESULTS: The genome-wide association study identified a highly suggestive locus that mapped to the 5′-flanking region of the CDCP1 (CUB [complement C1r/C1s, Uegf, and Bmp1] domain containing protein 1) gene (rs6773435; P =7.12×10 −7 ). The variant allele was associated with improved cardiac function and decreased CDCP1 transcription. CDCP1 expression was significantly upregulated in human cardiac fibroblasts (HCFs) in response to the PDGF (platelet-derived growth factor) signaling, and knockdown of CDCP1 significantly repressed HCF proliferation and decreased AKT (protein kinase B) phosphorylation. Transcriptomic profiling after CDCP1 knockdown in HCFs supported the conclusion that CDCP1 regulates HCF proliferation and mitosis. In addition, CDCP1 knockdown in HCFs resulted in significantly decreased expression of soluble ST2 (suppression of tumorigenicity-2), a prognostic biomarker for heart failure and inductor of cardiac fibrosis. CONCLUSIONS: CDCP1 may play an important role in myocardial recovery in recent-onset DCM and mediates its effect primarily by attenuating cardiac fibrosis.