228 research outputs found
Exploring Cellular Stress Response and Chaperones
Since the pioneering discovery of heat shock proteins in Drosophila by Ferruccio Ritossa in 1960s, a long and exciting journey has been undertaken by molecular biologists and researchers worldwide. Not only lower organisms like worms, yeast, amoeba, and flies but also eukaryotes share common cellular response signals to stressful conditions that can arise from the outside but also from the inside. Moreover, extraordinary interplay between nucleus and subcellular organelles, and between different organelles, like mitochondria and the endoplasmic reticulum called mitochondria-associated endoplasmic reticulum membranes (MAMs), are involved in aging and human diseases like obesity, diabetes, inflammation, neurodegeneration, autoimmune diseases, atherosclerosis, and cancer. Actually, we know that to hit abnormal proteostasis and lipid exchanges in the endoplasmic reticulum is crucial to best guide effective therapies or discover new drugs. Indeed, restoration or impairment of endoplasmic reticulum shape and function lead to cellular homeostasis by autophagy or to final death generally by apoptosis or pyroptosis. This Special Issue collects current valuable articles or reviews on cellular stress research and each contribution opens a new window for further studies and hypothesis. I hope that readers interested in this fascinating topic may be stimulated to know more and more
Different effects of Cyclosporine A and melatonin treatment on the expression of stress protein in rat liver.
MELATONIN INFLUENCES SMALL HEAT SHOCK PROTEINS EXPRESSION IN CYCLOSPORINE A INDUCED NEPHROPATHY IN RATS
Morphological and biochemical studies on aging and autophagy
To maintain health in the elderly is a crucial objective for modern medicine that involves both basic and clinical researches. Autophagy is a fundamental auto-cannibalizing process that preserves cellular homeostasis and, if altered, either by excess or defect, greatly changes cell fate and can result in incapacitating human diseases. Efficient autophagy may prolong lifespan, but unfortunately this process becomes less efficient with age. The present review is focused on the close relationship between autophagy and age-related disorders in different tissues/organs and in transgenic animal models. In particular, it comments on the up to date literature on mechanisms responsible for age-related impairment of autophagy. Moreover, before discussing about these mechanisms, it is necessary to describe the metabolic autophagic regulation of autophagy and the proteins involved in this process. At the end, these data would summarize the autophagic link with aging process, as important tools in the future biogerontology scenario
Resveratrol and Sirt 1 activators for the treatment of aging and age-related diseases
Reduced calorie intake is a religious and medical practice known since very old times,
but its direct influence on life span in all organisms, included humans, has been demonstrated
in the modern era. Not only periodic fasting, but also natural or synthetic
compounds that mimic this phenomenon are growing to slow aging and the onset of
chronic morbidities. Resveratrol (RSV), a plant polyphenol, is an elixir of longevity for
simple organisms and preclinical rodent models even if a beneficial role in humans is still
debated. Its main rejuvenating mechanism copes with the activation of specific longevity
genes called sirtuins. Among seven known mammalian sirtuins, sirtuin 1 is the most
studied. This pleiotropic nicotinamide adenine dinucleotide (NAD)-based deacetylase
maintains longevity by removing acetyl group in nuclear histones, transcription factors,
and other DNA repairing proteins. Actually, an exciting challenge is to discover and test
novel sirtuin 1 activators to extend life span and to treat age-associated disabilities. This
chapter updates on the antiaging effect of RSV and sirtuin 1 activators in experimental
animals and in humans. Finally, pros and cons on RSV analogues and sirtuin 1 activators
tested in preclinical and clinical trials to hamper neurological deficit, cardiovascular
complications, diabetes, bone and muscle deterioration, and cancer are discussed
Impact of melatonin on skeletal muscle and exercise
Skeletal muscle disorders are dramatically increasing with human aging with enormous
sanitary costs and impact on the quality of life. Preventive and therapeutic tools to limit the onset and
progression of muscle frailty include nutrition and physical training. Melatonin, the indole
produced at nighttime in the pineal and extra-pineal sites in mammalians, has recognized anti-aging,
anti-inflammatory, and anti-oxidant properties. Mitochondria are the favorite target of melatonin,
which maintains them efficiently, scavenging free radicals and reducing oxidative damage. Here,
we discuss the most recent evidence of dietary melatonin efficacy in age-related skeletal muscle
disorders in cellular, preclinical, and clinical studies. Furthermore, we analyze the emerging impact
of melatonin on physical activity. Finally, we consider the newest evidence of the gut–muscle axis
and the influence of exercise and probably melatonin on the microbiota. In our opinion, this review
reinforces the relevance of melatonin as a safe nutraceutical that limits skeletal muscle frailty and
prolongs physical performance
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