In many tissues, homeostatic tissue maintenance and regenerative responsiveness to injury depend on tissue-specific stem cells. When residing in the tissues, stem cells display tissue-specific differentiation patterns, and their ability to balance quiescence with proliferative activity appears to be critical for their survival and turnover. Interestingly, the life-long persistence of stem cells in the organism makes them particularly susceptible to the accumulation of cellular damage, which ultimately can lead to cell death, senescence, or loss of regenerative function, ultimately leading to compromising normal tissue physiology. Indeed, stem cells in many tissues have been found to undergo profound changes with age, exhibiting reduced responsiveness to tissue injury, dysregulation of proliferative activities, and declining functional capacities. These changes translate into reduced effectiveness of cell replacement and tissue regeneration in aged organisms.
Stem Cell Aging is affected by many different cell-intrinsic and cell-extrinsic pathways cross-talk which is crucial in the determination of stem cell function. Therefore, it is challenging to place particular weight on any one pathway concerning aging mechanisms. Our goal is to discuss certain signals that appear to be more broadly involved than others, at least given available research, and this could imply that they are more important regulators of aging stem cells. Having this in mind, I aim to create sub-sections to tackle each key component separately. These sub-sections include, for example, proteostasis, DNA damage, metabolism, epigenetic memory, cellular extracellular niche, and interventions.
We welcome submissions from Original research, Review articles, Rapid communications, and Case studies which may include (but are not limited to) the following:
•How the failure of proteostasis contributes to the age-dependent decline in adult stem cell function. Special interests are regulation of global protein translation, protein degradation, and protein folding.
•How do adult-specific stem cells differentially deal with DNA damage and what is the impact of genotoxic stress on specific adult stem cell fate.
•The factors that impact the balance between glycolysis, mitochondrial oxidative phosphorylation, fatty acid oxidation, and oxidative stress during the maturation of adult stem cells, and over the course of aging.
•Recent advances in the role of epigenetic factors in adult stem cell function and tissue homeostasis.
•The main characteristics of stem cell niches in these different tissues, highlighting the various components influencing adult stem cell activity.
•The advances and challenges in the development of adult stem cell-based therapies, with a focus on the use of stem cells in regenerative treatment modalities in several diseases.
In many tissues, homeostatic tissue maintenance and regenerative responsiveness to injury depend on tissue-specific stem cells. When residing in the tissues, stem cells display tissue-specific differentiation patterns, and their ability to balance quiescence with proliferative activity appears to be critical for their survival and turnover. Interestingly, the life-long persistence of stem cells in the organism makes them particularly susceptible to the accumulation of cellular damage, which ultimately can lead to cell death, senescence, or loss of regenerative function, ultimately leading to compromising normal tissue physiology. Indeed, stem cells in many tissues have been found to undergo profound changes with age, exhibiting reduced responsiveness to tissue injury, dysregulation of proliferative activities, and declining functional capacities. These changes translate into reduced effectiveness of cell replacement and tissue regeneration in aged organisms.
Stem Cell Aging is affected by many different cell-intrinsic and cell-extrinsic pathways cross-talk which is crucial in the determination of stem cell function. Therefore, it is challenging to place particular weight on any one pathway concerning aging mechanisms. Our goal is to discuss certain signals that appear to be more broadly involved than others, at least given available research, and this could imply that they are more important regulators of aging stem cells. Having this in mind, I aim to create sub-sections to tackle each key component separately. These sub-sections include, for example, proteostasis, DNA damage, metabolism, epigenetic memory, cellular extracellular niche, and interventions.
We welcome submissions from Original research, Review articles, Rapid communications, and Case studies which may include (but are not limited to) the following:
•How the failure of proteostasis contributes to the age-dependent decline in adult stem cell function. Special interests are regulation of global protein translation, protein degradation, and protein folding.
•How do adult-specific stem cells differentially deal with DNA damage and what is the impact of genotoxic stress on specific adult stem cell fate.
•The factors that impact the balance between glycolysis, mitochondrial oxidative phosphorylation, fatty acid oxidation, and oxidative stress during the maturation of adult stem cells, and over the course of aging.
•Recent advances in the role of epigenetic factors in adult stem cell function and tissue homeostasis.
•The main characteristics of stem cell niches in these different tissues, highlighting the various components influencing adult stem cell activity.
•The advances and challenges in the development of adult stem cell-based therapies, with a focus on the use of stem cells in regenerative treatment modalities in several diseases.