Cellular Contributors and Consequences of Protein Misfolding and Aggregation: Volume II

Given the success of Volume I of this Research Topic, and how rapid the subject area is evolving, we are pleased to announce the launch "Cellular Contributors and Consequences of Protein Misfolding and Aggregation - Volume II"Proper protein folding to its 3D structure is essential for cellular homeostasis. Protein misfolding and aggregation are believed to be major driving factors of neurological diseases and diabetes, cancer, and age-associated diseases. Understanding why specific proteins misfold, aggregate, or form biomolecular condensates, and why only certain cell types are vulnerable, is crucial in unraveling the mechanistic basis of the disease. Most of the protein-folding diseases that have been identified are known for their shared disease-initiating mechanisms. Cell membrane disruption, organellar stress, self-seeding or cross-seeding of protein aggregates, and prion-like cell-to-cell transmission are some of the well-described common pathological mechanisms. Two major questions that remain unaddressed include: What dictates aggregation of certain proteins in certain cells and which cellular machineries regulate this process? In order to devise therapeutic measures for proteinopathies, it is necessary to: 1) determine the causes of the protein folding problems, and 2)examine the cellular damage caused by the protein oligomers, aggregates, or condensates.This Research Topic is aimed at providing an understanding of 1) the causal factors of protein misfolding, aggregation and/or condensation in cells, 2) how protein misfolding and protein aggregation affect cellular processes and organelles in specific cell types leading to human diseases, and 3) protective cellular mechanism to tackle proteotoxicity in proteinopathies.• Protein misfolding and degenerative diseases• Biomolecular condensates in proteinopathies• Protein folding diseases, ER stress and calcium homeostasis• Oxidative stress and mitochondrial dysfunction in proteinopathies• Cell type specificity of protein aggregation and toxicity• Autophagy and proteostasis• Protein degradation machineries in diseases• Protein homeostasis failure in aging disorders• Pharmacological enhancement of protein folding and degradation Topic editors: Anoop Arunagiri, Emily Sontag, Arunkumar Venkatesan, Maria Del Carmen Fernandez-Ramirez Source: https://www.frontiersin.org/research-topics/83263/cellular-contributors-and-consequences-of-protein-misfolding-and-aggregation-volume-ii