Cellular Stress Response in Health and Disease

Dear Colleagues,

Stress is implied in cellular life, and according to the “hormesis principle”, a mild cellular stress is sometimes useful to best react against a more severe insult. Historically, we owe the seminal discovery of the “heat stress response” to the Italian scientist Ferruccio Ritossa in the 1960s, which demonstrated an intense transcriptional activity in chromosomal puffs in heated Drosophila salivary glands. Afterwards, heat shock proteins (HSPs) have been characterized not only in hyperthermia but also in the response to environmental, metabolic, or toxic inputs. In aging, a stressful reaction occurs because stress proteins are reduced. However, HSPs are not only inside cells but also in the extracellular environment in cancer, inflammation, and intercellular communication through exosomes. Besides classical HSPs, when homeostasis is disrupted, abnormal endoplasmic reticulum (ER) and mitochondrial stress triggers the unfolded protein response (UPR). This mechanism is dramatically involved in the pathogenesis of cancer, neurodegenerative diseases like Alzheimer’s, Parkinson’s, and amyotrophic lateral sclerosis, in retinal damage, and in cardiovascular and metabolic morbidities. So, strategies aimed at modulating ER stress or mitochondrial response are crucial. This Special Issue offers an Open Access forum that aims to bring together a collection of original research and review articles addressing the expanding field of cellular stress response and modulation. We hope to provide a stimulating resource for the fascinating subject of cell stress research. Suggested potential topics may be: hormesis; ER stress and mitochondrial stress in diseases; the role of HSPs in exercise and in longevity; molecular chaperones as therapeutic targets; exosomes and HSPs; and new models to study stress response

Dr. Alessandra Stacchiotti
Guest Editor

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