Decoding the Noncoding Transcripts in Human Heart Failure

Heart failure (HF) is a complex disease with a broad spectrum of pathological features. Despite significant advancement in clinical diagnosis through improved imaging modalities and hemodynamic approaches, reliable molecular signatures for better differential diagnosis and for better monitoring of heart failure progression remain elusive. The few known clinical biomarkers for heart failure, such as plasma BNP and Troponin, have been shown to have limited use in defining the etiology or prognosis of the disease1, 2. Consequently, current clinical identification and classification of heart failure remain descriptive, largely based on functional and morphological parameters. Therefore, defining the pathogenic mechanisms for hypertrophic vs. dilated or ischemic vs. non-ischemic cardiomyopathies in the failing heart remain a major challenge to both basic science and clinic researchers. In recent years, mechanical circulatory support using left ventricular assist devices (LVAD) has assumed a growing role in the care of patients with end-stage HF 3. During the earlier years of LVAD application as a bridge to transplant, it became evident that some patients exhibit substantial recovery of ventricular function, structure and electrical properties4. This led to the recognition that reverse remodeling is potentially an achievable therapeutic goal using LVAD. However, the underlying mechanism for the reverse remodeling in the LVAD treated hearts is unclear and its discovery would likely hold great promise to halt or even reverse the progression of heart failure.