Dear Colleagues,

Heart failure (HF) remains a leading cause of the premature death of in-patients with established cardiovascular (CV) disease. Although the number of new cases of HF with reduced ejection fraction (HFrEF) demonstrates a trend to decline in developed countries due to serious success in the implementation of complex management and prevention of CV risk factors, the prevalence of HF with preserved ejection fraction (HFpEF) continues to grow worldwide. It is suggested to be related to age, gender, spreading metabolic comorbidities including diabetes mellitus, and other conventional CV risk factors such as hypertension and dyslipidemia. In fact, primary cause and signature CV risk factors of adverse cardiac remodeling sufficiently distinguish HFrEF and HFpEF. HFrEF is closely associated with myocardial cell loss due to necrosis resulting from ischemia, inflammation, and apoptosis, whereas HFpEF is frequently result of microvascular inflammation, myocardial hypertrophy, rearrangement of extracellular matrix and interstitial fibrosis. In fact, clinical presentation and the risk of untoward course and poor outcomes exhibit a strict similarity in patients with both phenotypes of HF. However, impaired physical activity due to muscle weakness, skeletal myopathy, muscle atrophy, and finally cachexia are the attributive factors for HF progression, increased CV mortality, and decreased quality of life. It has been hypothesized that skeletal muscle metabolism and weakness are linked with adipose tissue homeostasis and cardiac structure and function through the endogenous system of myokines and adipocytokines—a profile which has a significant relation to HF phenotypes and their etiology.

The aim of this Special Issue is to publish new insights into future diagnostic and therapeutic approaches by synthesizing the current knowledge on the underlying molecular mechanisms by which myokines and adipocytokines regulate adverse cardiac remodeling and predict heart failure.

Topics of interest for the Special Issue include but are not limited to:

• Risk factors and predictors of adverse cardiac remodeling;
• Adaptive and maladaptive cardiac remodeling;
• Underlying molecular mechanisms of adverse cardiac remodeling;
• Endothelial dysfunction and myokine profile;
• Adipose tissue dysfunction and microvascular inflammation;
• Myokine and adipocytokine in metabolic comorbidities among heart failure patients;
• Plasma omics profiling in heart failure;
• Myokines signature in diabetes mellitus cardiomyopathy;
• Myokine-related clinical signs in heart failure;
• Myokine myopathy and cardiac cachexia;
• Osteoporosis in heart failure. 

We invite the submission of original research articles, narrative and systemic reviews, and communications.

Prof. Dr. Alexander E. Berezin
Prof. Dr. Michael Lichtenauer
Prof. Dr. Eric J. Stöhr
Guest Editors

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• adverse cardiac remodeling
• cardiac dysfunction
• heart failure
• underlying pathophysiological mechanisms
• visualization
• biomarkers
• myokines
• adipocytokines
• management