title: DUSPs as critical regulators of cardiac hypertrophy.
abstract: This commentary highlights the research presented by Li et al. [15]. In this issue of Clinical Science, which demonstrates that dual specific phosphatase 12 (DUSP12), through JNK1/2 inhibition, alleviates cardiac hypertrophy in response to pressure overload, making it a potential therapeutic target.
authors.affiliation: Center of Translational Medicine and Department of Pharmacology, Lewis Katz Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.
authors.forename: Douglas G
authors.initials: DG
authors.lastname: Tilley
authors.affiliation: Cardiovascular Research Center and Department of Physiology, Lewis Katz Temple University School of Medicine, Philadelphia, PA 19140, U.S.A. sabri@temple.edu.
authors.forename: Abdelkarim
authors.initials: A
authors.lastname: Sabri
mesh_terms: D000818:Animals; D006332:Cardiomegaly / Q000201:enzymology* / Q000235:genetics / Q000503:physiopathology; D054637:Dual-Specificity Phosphatases / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D032383:Myocytes, Cardiac / Q000201:enzymology; D015398:Signal Transduction
chemical_list: D048031:JNK Mitogen-Activated Protein Kinases; D054637:Dual-Specificity Phosphatases
keywords: DUSP12; JNK1/2; cardiac hypertrophy