期刊
NATURE CLINICAL PRACTICE CARDIOVASCULAR MEDICINE
卷 5, 期 4, 页码 208-218出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncpcardio1127
关键词
apoptosis; calcium; cardiac; necrosis; nitric oxide
资金
- NHLBI NIH HHS [R01 HL084498-01A2, R01 HL084498, R01 HL079283, R01 HL048848] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL084498, R01HL079283, R01HL048848] Funding Source: NIH RePORTER
Acute decompensated heart failure (ADHF) is responsible for more than I million hospital admissions each year in the US. Clinicians and scientists have developed therapeutic strategies that reduce mortality in patients with chronic heart failure (HF). Despite the widely appreciated magnitude of the ADHF problem, there is still a critical gap in our understanding of the cellular mechanisms involved and effective treatment strategies for hospitalized patients. Irrespective of the etiology, patients with ADHF present with similar symptoms (e.g. edema, altered hemodynamics and congestion) as multiple signaling pathways converge in a common phenotypic presentation. Investigations have shown that patients with ADHF have increased catecholamine levels, which cause chronic stimulation of P-adrenergic receptors. This overstimulation leads to chronic G-protein activation and perturbations in myocyte signaling, as the patient's heart attempts to adapt to progressive HE Over time, these compensatory signaling mechanisms ultimately fail, and maladaptive signaling prevails with progressive worsening of symptoms. This Review summarizes some of the changes that occur during chronic adrenergic stimulation, and examines how downstream contractile dysfunction and myocyte death can alter the prognosis of patients with HF hospitalized for acute events.
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