Globally, the number of adults over the age of 65 is expected to rise from 617 million today to more than 2 billion by 2050, representing 20 percent of the world's population. With the increase in the number of the older population, aging has become the major risk factor for all age-related chronic diseases. Therefore, abetter understanding of the mechanism of aging could vastly improve the quality of life of older subjects.
The study of aging has experienced unprecedented advances in the last 15 years, especially with the discovery that the rate of aging is controlled, at least in part, by genetic pathways and biochemical processes which are evolutionary conserved.. As a complex, multifaceted process that causes a wide range of functional decline, aging has some common hallmarks, such as genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. Analyzing and understanding this complex signaling network remains a major challenge.
Protein homeostasis or proteostasis is a dynamic process in which cells regulate protein synthesis, folding, transport, post-translational modification, and degradation. The main participants in protein homeostasis are chaperones and two proteolytic systems, the ubiquitin-proteasome and lysosomal-autophagy systems.. Overall, this integrated pathway network helps maintain the stability and function of the cellular proteome by preventing the accumulation of mistranslated, aggregated, misfolded, or damaged proteins. A large body of evidence supports a close relationship between protein homeostasis and healthy aging. Although a gradual loss of protein homeostasis with age has been detected in most organisms, species with the longest lifespans have been shown to have a more stable proteome. Interestingly, most of the interventions that slow aging in experimental models are associated with improved proteostasis, and in many cases these interventions also show autophagy activation. . For example, caloric restriction, rapamycin, metformin, resveratrol, and spermidine, known for their ability to extend lifespan, have all been shown to activate autophagy directly, albeit through different mechanisms.
This Research Topic will focus on the regulation of proteostasis in the process of aging. In addition, it seeks studies answering the following questions:
What is the association relationship between proteostasis and aging?
What is the relationship between proteostasis and other hallmarks of aging?
What signaling pathways are maintained by homeostasis in healthy or disease conditions?
How can we improve aging and age-related diseases by targeting protein homeostasis?
Areas to be covered may include, but are not limited to:
• Key factors affecting proteostasis
• Relationship association between proteostasis and aging
• Mechanisms of proteostasis collapse leading to aging
• New methods for detecting and analyzing cellular proteostasis
• The relationship between proteostasis and other hallmarks of aging, such as deregulated nutrient-sensing, and mitochondrial dysfunction.
Globally, the number of adults over the age of 65 is expected to rise from 617 million today to more than 2 billion by 2050, representing 20 percent of the world's population. With the increase in the number of the older population, aging has become the major risk factor for all age-related chronic diseases. Therefore, abetter understanding of the mechanism of aging could vastly improve the quality of life of older subjects.
The study of aging has experienced unprecedented advances in the last 15 years, especially with the discovery that the rate of aging is controlled, at least in part, by genetic pathways and biochemical processes which are evolutionary conserved.. As a complex, multifaceted process that causes a wide range of functional decline, aging has some common hallmarks, such as genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. Analyzing and understanding this complex signaling network remains a major challenge.
Protein homeostasis or proteostasis is a dynamic process in which cells regulate protein synthesis, folding, transport, post-translational modification, and degradation. The main participants in protein homeostasis are chaperones and two proteolytic systems, the ubiquitin-proteasome and lysosomal-autophagy systems.. Overall, this integrated pathway network helps maintain the stability and function of the cellular proteome by preventing the accumulation of mistranslated, aggregated, misfolded, or damaged proteins. A large body of evidence supports a close relationship between protein homeostasis and healthy aging. Although a gradual loss of protein homeostasis with age has been detected in most organisms, species with the longest lifespans have been shown to have a more stable proteome. Interestingly, most of the interventions that slow aging in experimental models are associated with improved proteostasis, and in many cases these interventions also show autophagy activation. . For example, caloric restriction, rapamycin, metformin, resveratrol, and spermidine, known for their ability to extend lifespan, have all been shown to activate autophagy directly, albeit through different mechanisms.
This Research Topic will focus on the regulation of proteostasis in the process of aging. In addition, it seeks studies answering the following questions:
What is the association relationship between proteostasis and aging?
What is the relationship between proteostasis and other hallmarks of aging?
What signaling pathways are maintained by homeostasis in healthy or disease conditions?
How can we improve aging and age-related diseases by targeting protein homeostasis?
Areas to be covered may include, but are not limited to:
• Key factors affecting proteostasis
• Relationship association between proteostasis and aging
• Mechanisms of proteostasis collapse leading to aging
• New methods for detecting and analyzing cellular proteostasis
• The relationship between proteostasis and other hallmarks of aging, such as deregulated nutrient-sensing, and mitochondrial dysfunction.