Mechanisms of Ghrelin Anti-Heart Failure: Inhibition of Ang II-Induced Cardiomyocyte Apoptosis by Down-Regulating AT1R Expression

Yang, Chunyan; Liu, Zhonghui; Liu, Kai; Yang, Ping

doi:10.1371/journal.pone.0085785

Cited by 45 publications

(36 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Interestingly, ghrelin by down-regulating angiotensin 1 receptor inhibited Angiotensin II-induced apoptosis of cardiomyocytes in vitro, thus playing a role in preventing heart failure [231].…”

Section: Ghrelin-associated Peptidesmentioning

confidence: 99%

“…With chronic use of ACE-I the incidence of AMI is reduced [323,324], and apart from more favorable hemodynamics, their antioxidant properties and pro-bradykinin, pro-nitric oxide effects may contribute to such benefit [240], thus limiting the possibility of additional protection by conditioning protocols [118]. Moreover statins, nitrates, and antidiabetic drugs may treat risk factors thus influencing cardioprotection by modifying cellular signaling involved in protection [231].…”

Section: Conclusion: the Future Of Pharmacological Conditioningmentioning

confidence: 99%

See 1 more Smart Citation

Endogenous Cardioprotective Agents: Role in Pre and Postconditioning

Penna¹,

Granata²,

Tocchetti³

et al. 2015

CDT

View full text Add to dashboard Cite

Cardiovascular diseases (CVD) are the leading cause of death, chronic illness and disability in Western countries. The most common cause of CVD derives from the harmful effects of acute myocardial ischemia and subsequent reperfusion injury. Cardioprotection against acute ischemia/ reperfusion injury is made possible by the "conditioning protocols." Conditioning is obtained by applying a few periods of brief ischemia and reperfusion in the event of prolonged (index) ischemia that may cause myocardial infarction. Whilst the conditioning stimulus is applied before the index ischemia in ischemic pre-conditioning, it is applied after the event in post-conditioning. Pre and post- conditioning stimuli can be applied in a different/remote organ (remote pre- and post-conditioning); in this case conditioning stimulus can also be applied during the index event, in the so called remote per-conditioning. All these endogenous cardioprotective strategies recruit endogenous cytoprotective agents and factors that elicit specific cardioprotective pathways. Here, we discuss many of these cardioprotective factors compared to literature and highlight their main characteristics and mechanisms of action. Enphasis is given to endogenous cardioprotective agents acting or not on surface receptors, including chromogranin A derivatives, ghrelin-associated peptides, growth factors and cytokines, and to microvesicles and exosomes. Moreover the cardioprotective effects of gasotransmitters nitric oxide, hydrogen sulphide and carbon monoxide are reviewed. The possible clinical translation of these knowledge for future successful therapies is briefly and critically discussed.

show abstract

Section: Ghrelin-associated Peptidesmentioning

confidence: 99%

Section: Conclusion: the Future Of Pharmacological Conditioningmentioning

confidence: 99%

Endogenous Cardioprotective Agents: Role in Pre and Postconditioning

Penna¹,

Granata²,

Tocchetti³

et al. 2015

CDT

View full text Add to dashboard Cite

show abstract

“…This is mediated by interference with myokines (FGF-21) and local hormones and growth-factors such as myostatin [33], IGF-1 [34], ghrelin [35] and leptin [36]. Thus, ethanol decreases the myocyte proliferation rate probably by myostatin up-regulation [33] and modifies the mechanisms of cardiac plasticity [37].…”

Section: Pathogenic Factorsmentioning

confidence: 99%

Alcoholic Cardiomyopathy: Old and New Insights

Fernández‐Solà¹,

Riba²

2017

J Alcohol Drug Depend

View full text Add to dashboard Cite

Alcohol cardiomyopathy (ACM) is a chronic dilated heart disease with decreased left ventricular ejection fraction that may be detected in one-fourth of high-dose alcohol consumers. It causes progressive diastolic and systolic dysfunction, supra and ventricular arrhythmias leading to heart failure and increased mortality. The main etiological factor for ACM is ethanol consumption that affects the myocardium in a dose-dependent manner. The mechanisms of ACM are diverse, synchronic and synergistic. Alcohol alters the channel and receptor structure of the cell membrane, decreases intracellular calcium transients, increases oxidative and inflammatory damage, decreases structural protein synthesis and interferes with excitation-contraction coupling mechanisms. Subjects with excessive alcohol consumption may have a subclinical cardiomyopathy with atrial and LV diastolic dysfunction measured by echocardiography or cardiac MR. Subclinical LV dysfunction may progress and later appear clinical features of heart failure. Cardiac myocytes adapt to ethanol aggression by cell and nuclear hypertrophy and dilatation of heart chambers. Progressive myocyte structure disarray and apoptosis produce myocyte loss, hypertrophy of the remaining cells, subendocardial and interstitial fibrosis and low-degree myocyte regeneration. In addition, ethanol also interferes with cardiac repair and adaptation mechanisms. Thus, local cardiomyokines (FGF-21) and growth factors (myostatin, IGF-1, leptin) are modified by ethanol, limiting cardiac remodeling and myocyte regeneration, and leading to abnormal hypertrophy and eccentric ventricle dilatation. This imbalance between aggression and protection mechanisms induces progressive myocyte loss and heart dysfunction. Alcohol abstention is the main goal in ACM, although control drinking (<-60 g/day) may allow recovery of LV function. Monitoring of systemic mediated alcohol-damage, and correction of vitamin and ion deficiencies is needed. Heart failure in ACM should be treated similar to other dilated cardiomyopathies. Heart transplantation is limited to subjects without other organ damage who are able to abstain from alcohol. New preventive and therapeutic strategies are under development to decrease alcohol-mediated myocyte damage and increase heart protective and repair mechanisms.

show abstract

“…Although the precise mechanism of CHF involves a variety of agents and conditions, a gradual decrease in cardiomyocyte number is one of the most important pathogenic factors, according to previous studies . In particular, accumulating evidence in both human and animal models showed that one of the predominant forms of cardiomyocyte loss during CHF is cardiomyocyte apoptosis, an important mode of programmed cell death, which could be lethal even at too low levels . In this regard, the possibility of limiting cardiac muscle loss by inhibiting cardiomyocyte apoptosis might have important implications for the treatment of CHF …”

Section: Introductionmentioning

confidence: 99%

“…[7][8][9] In particular, accumulating evidence in both human and animal models showed that one of the predominant forms of cardiomyocyte loss during CHF is cardiomyocyte apoptosis, an important mode of programmed cell death, which could be lethal even at too low levels. [10][11][12] In this regard, the possibility of limiting cardiac muscle loss by inhibiting cardiomyocyte apoptosis might have important implications for the treatment of CHF. 7 Thoracic epidural anesthesia (TEA) is an effective anesthetic method, which has been widely used in cardiac surgery for its cardiac protective effect.…”

Section: Introductionmentioning

confidence: 99%