Molecular Insights in Heart Failure

Dear Colleagues,

Heart failure remains a disease of epidemic proportion affecting people equally in both industrialized and non-industrialized countries. The past several years have seen the evaluation and approval of exciting new treatments for patients with heart failure including the combination of a neprilysin inhibitor and an angiotensin receptor antagonist, SGLT2 inhibitors, and the use of acetazolamide, an old diuretic used previously for the treatment of high-altitude sickness. In addition, clinical investigations have expanded our ability to phenotype patients by adding more precise definitions for the various stages of heart failure such that patients are now considered as having heart failure with reduced ejection fraction, heart failure with preserved ejection and the new distinction of heart failure with mid-range ejection fraction. Despite the development of more precise definitions for the different phenotypes of heart failure and new treatment algorithms that fit the various therapies with specific patient populations, the overall morbidity and mortality of the disease remains consequential as none of these agents cure the disease and some improve symptoms but have no effect on survival. However, the science of heart failure is also progressing at a rapid pace as investigators have begun to use the rapidly developing fields of molecular and cellular biology to identify genetic causes for heart muscle disease, to link changes at the molecular level with altered cardiac phenotypes and to develop small molecules that effectively modify the cellular and biologic abnormalities that are causative of various forms of heart failure. Perhaps the best example of precision medicine in the area of cardiovascular disease was the development of mavacamten, a novel first-in-class molecule that is a selective and reversible inhibitor of the cardiac myosin ATPase that successfully treats patients with symptomatic heart failure secondary to obstructive hypertrophic cardiomyopathy.

In this Special Issue on “Molecular Insights in Heart Failure,” we will review the molecular and cellular insights that led to the development of the new classes of heart failure therapeutics including the role of neurohormonal activation and natriuretic peptides in the development and treatment of heart failure, the molecular biology of the contractile elements including myosin, and how an understanding of the molecular and cellular biology of the contractile elements and the specific changes that occur in patients with hereditary hypertrophic cardiomyopathy led to the development of mavacamten. However, we will dedicate a large portion of this Special Issue to understanding how unique heritable genetic defects have led to the development of new and novel treatments for heart muscle disease. We seek discussions of ongoing studies of heart failure populations to identify novel genetic variants that provide new therapeutic targets and molecular studies of putatively causative genetic variants to better understand the molecular pathways through which these genetic variants alter the normal physiology. Finally, we seek submissions of manuscripts that focus on the use of gene and cell therapy to alter the adverse genotypes in order to normalize precise pathways and in so doing improve the function of the heart and the survival of patients and family members.

Prof. Dr. Arthur M. Feldman
Guest Editor

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• heart failure
• neurohormonal activation
• natriuretic peptides
• myosin
• mavacamten
• contractile elements
• gene and cell therapy
• monoclonal genetic disease
• autophagy
• apoptosis
• calcium homeostasis
• channelopathies
• single cell proteomics
• single cell sequencing
• RNA seq
• genetics
• haplo-insufficiency
• TNF alpha
• TNF receptor
• cellular metabolism
• mitochondria
• mitochondrial damage
• caspases
• cytokine receptors
• pro-inflammatory cytokines
• membrane potential
• sex-related variation
• survival
• gene vectors
• BAG3
• BAG1