The Role of Cardiokines in Heart Diseases: Beneficial or Detrimental?

Wu, Yeshun; Zhu, Bin; Luo, Ailin; Yang, Ling; Yang, Chun

doi:10.1155/2018/8207058

Cited by 27 publications

(26 citation statements)

References 142 publications

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“…Subjects with ACM who continue in high-dose ethanol consumption have a bad prognosis, with repeated episodes of heart failure and ventricular arrhythmias leading to a 10% increase in annual mortality rate [56,61]. New strategies aiming to control apoptosis, autophagy and pathological heart remodeling, and increase myocyte regeneration may be promising in the near future [112,133]. However, areas of uncertainty in this complex disease are still present and should be further explored [30].…”

Section: Discussionmentioning

confidence: 99%

“…The heart output is progressively lower in a dose-dependent relationship with the lifetime accumulated total dose of alcohol consumed [38]. Several growth factors and cardiomyokines exert an autocrine or paracrine effect that tries to compensate for this heart damage [119,133]. Antioxidant, anti-inflammatory, anti-apoptotic, and antifibrogenic mechanisms try to avoid myocyte necrosis and heart fibrosis [14,30,58].…”

Section: Cardiac Hypertrophy and Remodeling In Acmmentioning

confidence: 99%

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The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Fernández‐Solà

2020

Nutrients

105

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Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition. The ACM prognosis depends on the degree of persistent ethanol intake. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.

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Section: Discussionmentioning

confidence: 99%

Section: Cardiac Hypertrophy and Remodeling In Acmmentioning

confidence: 99%

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Fernández‐Solà

2020

Nutrients

105

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“…Increasing evidence suggests that the heart synthesizes and secretes proteins referred to as cardiokines, which are involved in the inter-cellular and inter-organ communication [118]. More than 16 cardiokines have been identified, including the atrial natriuretic factor (ANF), BNP, transforming growth factor-β1 (TGF-β1), angiotensin II, and proinflammatory cytokines which are known to play physiological and pathological role in cardiac fibrosis, apoptosis, and metabolism [119].…”

Section: The Heart-liver Axismentioning

confidence: 99%

Relationship between Heart Disease and Liver Disease: A Two-Way Street

Hadi

Vincenzo

Rossato

2020

Cells

103

125

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In clinical practice, combined heart and liver dysfunctions coexist in the setting of the main heart and liver diseases because of complex cardiohepatic interactions. It is becoming increasingly crucial to identify these interactions between heart and liver in order to ensure an effective management of patients with heart or liver disease to provide an improvement in overall prognosis and therapy. In this review, we aim to summarize the cross-talk between heart and liver in the setting of the main pathologic conditions affecting these organs. Accordingly, we present the clinical manifestation, biochemical profiles, and histological findings of cardiogenic ischemic hepatitis and congestive hepatopathy due to acute and chronic heart failure, respectively. In addition, we discuss the main features of cardiac dysfunction in the setting of liver cirrhosis, nonalcoholic fatty liver disease, and those following liver transplantation.

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“…Cardiomyocytes are known to release "cardiokines" when under stress (as reviewed in Dewey et al (2016)). These cardiokines can impact proliferation, differentiation, and inflammation and can have both beneficial and detrimental effects, inhibiting and promoting apoptosis (as reviewed in Wu et al (2018)). Future work will examine the potential role for AnkB in regulating paracrine communication in H9c2 cells and cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

Ankyrin-B p.S646F undergoes increased proteasome degradation and reduces cell viability in the H9c2 rat ventricular cardiomyoblast cell line

Chen

Choi

Sanchez-Arias

et al. 2020

Biochem. Cell Biol.

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Ankyrin-B (AnkB) is scaffolding protein that anchors integral membrane proteins to the cardiomyocyte cytoskeleton. We recently identified an AnkB variant, AnkB p.S646F (ANK2 c.1937 C>T) associated with a phenotype ranging from predisposition for cardiac arrhythmia to cardiomyopathy. AnkB p.S646F exhibited reduced expression levels in the H9c2 rat ventricular-derived cardiomyoblast cell line relative to wildtype AnkB. Here, we demonstrate that AnkB is regulated by proteasomal degradation and proteasome inhibition rescues AnkB p.S646F expression levels in H9c2 cells, although this effect is not conserved with differentiation. We also compared the impact of wildtype AnkB and AnkB p.S646F on cell viability and proliferation. AnkB p.S646F expression resulted in decreased cell viability at 30 h after transfection, whereas we observed a greater proportion of cycling, Ki67-positive cells at 48 h after transfection. Notably, the number of GFP-positive cells was low and was consistent between wildtype AnkB and AnkB p.S646F expressing cells, suggesting that AnkB and AnkB p.S646F affected paracrine communication between H9c2 cells differentially. This work reveals that AnkB levels are regulated by the proteasome and that AnkB p.S646F compromises cell viability. Together, these findings provide key new insights into the putative cellular and molecular mechanisms of AnkB-related cardiac disease.

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The Role of Cardiokines in Heart Diseases: Beneficial or Detrimental?

Cited by 27 publications

References 142 publications

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

Relationship between Heart Disease and Liver Disease: A Two-Way Street

Ankyrin-B p.S646F undergoes increased proteasome degradation and reduces cell viability in the H9c2 rat ventricular cardiomyoblast cell line

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