Professor David A. Kass, MD, Department of Medicine, Division of Cardiology, Department of Biomedical Engineering, Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine speaks about Review: Cellular and molecular pathobiology of heart failure with preserved ejection fraction.Link to Review Article:https://www.nature.com/articles/s41569-020-00480-6Synopsis:Heart failure with retained ejection fraction (HFpEF) affects half of all heart failure patients worldwide, is becoming more common, is associated with significant morbidity and mortality, and has few successful therapies. The largest unmet medical need in cardiovascular disease is probably HFpEF. While HFpEF was once thought to be a haemodynamic disorder characterized by hypertension, cardiac hypertrophy, and diastolic dysfunction, the pandemics of obesity and diabetes mellitus have changed the HFpEF syndrome, which is now recognized as a multisystem disorder involving the heart, lungs, kidneys, skeletal muscle, adipose tissue, vascular system, immune and inflammatory systems. Since the disorder is more than just cardiac hypertrophy and hypertension with abnormal myocardial relaxation, HFpEF is difficult to model in laboratory animals. New animal models of haemodynamic and metabolic disease, as well as increased efforts to investigate human pathophysiology, are revealing new signaling mechanisms and possible therapeutic targets. We address the cellular and molecular pathobiology of HFpEF in this Study, with a specific emphasis on mechanisms related to the heart, as most research has been done on this organ. Other critical organ systems, such as the lungs, kidneys, and skeletal muscle, are also involved, as are attempts to characterize patients using systemic biomarkers and ongoing therapeutic efforts. Our aim is to build a map of the signaling pathways and mechanisms of HFpEF that are currently being studied, with the intention of creating more patient-specific therapies and enhancing clinical outcomes.Points to remember:* Historically, diastolic dysfunction, cardiac hypertrophy, and myocardial fibrosis have been the subject of research into the pathophysiology of heart failure with preserved ejection fraction (HFpEF).* Moreover, HFpEF is made up of a variety of factors that affect both systolic and diastolic heart function, as well as other organs and systems such as the lungs, kidneys, vasculature, adipose tissue, and skeletal muscle.* Preclinical studies, especially those that combine obesity and metabolic defects with haemodynamic and cardiac disease, as most patients with HFpEF do, are revealing novel molecular mechanisms and therapeutic targets.* Metabolic defects in fuel utilization and performance, inflammatory responses, lipotoxicity, pathological growth of myocytes, and lack of cytoprotective signaling are all proposed molecular and cellular abnormalities in HFpEF and those seen in diabetes mellitus and obesity.*New therapies are targeting pleiotropic signaling cascades to reverse improvements in metabolic, inflammatory, and pathological stress pathways, in addition to developing innovative haemodynamic treatments with drugs and devices. - Heart Failure and Cardiomyopathies - 371_600c9efaa3c99

David A. Kass, MD @HopkinsMedicine @hopkinsheart #HFpEF #HeartFailure #Cardiology #Heart #Research Review: Cellular And Molecular Pathobiology of Heart Failure With Preserved Ejection Fra...

David A. Kass, MD @HopkinsMedicine @hopkinsheart #HFpEF #HeartFailure #Cardiology #Heart #Research Review: Cellular And Molecular Pathobiology of Heart Failure With Preserved Ejection Fra...

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Professor David A. Kass, MD, Department of Medicine, Division of Cardiology, Department of Biomedical Engineering, Department of Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine speaks about Review: Cellular and molecular pathobiology of heart failure with preserved ejection fraction.

Link to Review Article:
https://www.nature.com/articles/s41569-020-00480-6

Synopsis:

Heart failure with retained ejection fraction (HFpEF) affects half of all heart failure patients worldwide, is becoming more common, is associated with significant morbidity and mortality, and has few successful therapies. The largest unmet medical need in cardiovascular disease is probably HFpEF. While HFpEF was once thought to be a haemodynamic disorder characterized by hypertension, cardiac hypertrophy, and diastolic dysfunction, the pandemics of obesity and diabetes mellitus have changed the HFpEF syndrome, which is now recognized as a multisystem disorder involving the heart, lungs, kidneys, skeletal muscle, adipose tissue, vascular system, immune and inflammatory systems. Since the disorder is more than just cardiac hypertrophy and hypertension with abnormal myocardial relaxation, HFpEF is difficult to model in laboratory animals. New animal models of haemodynamic and metabolic disease, as well as increased efforts to investigate human pathophysiology, are revealing new signaling mechanisms and possible therapeutic targets. We address the cellular and molecular pathobiology of HFpEF in this Study, with a specific emphasis on mechanisms related to the heart, as most research has been done on this organ. Other critical organ systems, such as the lungs, kidneys, and skeletal muscle, are also involved, as are attempts to characterize patients using systemic biomarkers and ongoing therapeutic efforts. Our aim is to build a map of the signaling pathways and mechanisms of HFpEF that are currently being studied, with the intention of creating more patient-specific therapies and enhancing clinical outcomes.

Points to remember:

* Historically, diastolic dysfunction, cardiac hypertrophy, and myocardial fibrosis have been the subject of research into the pathophysiology of heart failure with preserved ejection fraction (HFpEF).


* Moreover, HFpEF is made up of a variety of factors that affect both systolic and diastolic heart function, as well as other organs and systems such as the lungs, kidneys, vasculature, adipose tissue, and skeletal muscle.


* Preclinical studies, especially those that combine obesity and metabolic defects with haemodynamic and cardiac disease, as most patients with HFpEF do, are revealing novel molecular mechanisms and therapeutic targets.


* Metabolic defects in fuel utilization and performance, inflammatory responses, lipotoxicity, pathological growth of myocytes, and lack of cytoprotective signaling are all proposed molecular and cellular abnormalities in HFpEF and those seen in diabetes mellitus and obesity.


*New therapies are targeting pleiotropic signaling cascades to reverse improvements in metabolic, inflammatory, and pathological stress pathways, in addition to developing innovative haemodynamic treatments with drugs and devices.

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