Is RBM20 a Promising Target for HFpEF Therapy? Wei Guo Andrea R Sanchez Walk 10.25376/hra.7796618.v1 https://hra.figshare.com/articles/journal_contribution/Is_RBM20_a_Promising_Target_for_HFpEF_Therapy_/7796618 <div> <div> <div> <p>Heart Failure (HF) is a major public health issue with an estimated prevalence of over 37.7 million individuals worldwide [1], and remains the leading cause of morbidity, mortality, and hospitalization among adults and elderly [2,3]. In the USA, the total medical costs for patients with HF are expected to rise from US$20.9 billion in 2012 to $53.1 billion by 2030 [1]. About half of the patients with heart failure display preserved ejection fraction in contrast to the other half that present contractile dysfunction and a dilated heart (HF with reduced ejection fraction, HFrEF) [4,5]. Prototypical manifestations of heart failure with preserved ejection fraction (HFpEF), previously known as diastolic dysfunction, include increase in passive stiffness, insufficient recoil, and decrease in full relaxation [6]. Anaggregation of severalcontributors such as hypertension, metabolic syndrome, obesity and diabetes mellitus have been associated with the development of HFpEF [6]. Despite significant therapeutic improvements in the treatment of virtually all cardiac disorders, HF is an exception, in that its prevalence is rising, and its morbidity and mortality remain unacceptably high [7,8]. Currently, no effective therapies are available for HFpEF, at least with regard to major clinical events. Therefore, novel insights into pathophysiology and molecular mechanisms of HFpEF progression are required to develop novel therapeutic approaches.</p> <div> <div> <div> <p><br></p></div></div><div><div> </div> </div> </div> </div> </div> </div> 2019-03-03 18:12:05 Titin isoform switching Alternative splicing HFpEF RBM20 Biomarkers Cardiology (incl. Cardiovascular Diseases) Molecular Targets