Editorial: Molecular Mechanisms Involved in Heart Failure, Parkinson’s, and Alzheimer’s Diseases

Abstract

As life expectancy increases, chronic degenerative disorders such as heart failure (HF) and Alzheimer’s diseases are a growing pandemic for older adults. No available treatment can slow the progression of these diseases, and massive increases in health care costs are predicted in the coming years. Understanding the molecular mechanisms involved in the pathogenesis of such disorders would provide the basis for identifying druggable targets and facilitating novel treatments to prevent a decline in functional activities of daily living hence improving the quality of life of older adults. In this Research Topic, we provided updates on the most advanced knowledge on the interlinks between molecular triggering factors and signaling pathways and how they may influence almost every aspect of cardiovascular, neurological, and other chronic degenerative diseases. For instance, in their Review article, Gariballa and Ali explored the role of endoplasmic reticulum (ER) quality control mechanisms behind the pathogenesis of genetic diseases associated with alterations in the components of the TGFβ signaling pathway. As emerged in their analysis, the authors found that about 47 monogenic diseases are associated with genetic mutations in 24 out of 41 TGFβ components. The authors emphasized the urgency of establishing novel approaches in modulating the molecular pathway of mutant TGFβ components restoring their protein folding and trafficking as the final therapeutic goal. Importantly, protein misfolding is a well-recognized pathogenic mechanism involved in several disorders, and novel strategies to prevent such abnormal processes are needed. Therefore, the authors propose genetic manipulation of ER-associated protein degradation (ERAD) network to enhance mutant protein folding, localization, and activity as a novel strategy for preserving biologically functional properties of the TGFβ signaling pathway, counteracting the development of several chronic-degenerative disorders. Further, in their interesting analysis, Chen et al. described the pathogenetic role of proteinmisfolding in HF. Notably, these authors discussed the vital role of mitochondrial chaperones and proteases in the perturbation of protein homeostasis showing the mechanisms by which these influence cardiomyocyte functionality and survival. Importantly, alteration in protein folding has been recognized as a process leading to neurodegeneration and Alzheimer’s disease (AD) development (Uddin et al., 2021). Indeed, Edited by: William C. Cho, QEH, Hong Kong, SAR China