期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 119, 期 5, 页码 1082-1085出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI39262
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资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL062494, R01HL070250, R01HL079031, R01HL096652] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL 70250, R01 HL 079031, R01 HL 62494, R01 HL062494, R01 HL070250, R01 HL079031, R01 HL096652] Funding Source: Medline
Patients with systolic left ventricular dysfunction die progressively from congestive heart failure or die suddenly from cardiac arrhythmias. Myocardial hypertrophy is an early event in most forms of heart failure, but the majority of patients with myocardial hypertrophy do not develop heart failure. Developing improved therapies for targeting the cell signaling pathways that enable this deadly transition from early myocardial insult to heart failure and sudden death is a key goal for improving public health. In this issue of the JCI, Ling and colleagues provide new evidence that activation of the multifunctional Ca(2+)/calmodulin-dependent kinase II delta is a decisive step on the path to heart failure in mice (see the related article beginning on page 1230).
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