scholarly journals The Mechanism of Stem Cell Aging

2022 ◽  
Author(s):  
Liangyu Mi ◽  
Junping Hu ◽  
Na Li ◽  
Jinfang Gao ◽  
Rongxiu Huo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Tissue Repair ◽  
Molecular Mechanisms ◽  
Cell Aging ◽  
Therapeutic Application ◽  
Differentiation Potential ◽  
Stem Cell Aging ◽  
New Directions ◽  
Aging Mechanisms

AbstractStem cells have self-renewal ability and multi-directional differentiation potential. They have tissue repair capabilities and are essential for maintaining the tissue homeostasis. The depletion of stem cells is closely related to the occurrence of body aging and aging-related diseases. Therefore, revealing the molecular mechanisms of stem cell aging will set new directions for the therapeutic application of stem cells, the study of aging mechanisms, and the prevention and treatment of aging-related diseases. This review comprehensively describes the molecular mechanisms related to stem cell aging and provides the basis for further investigations aimed at developing new anti-stem cell aging strategies and promoting the clinical application of stem cells.

scholarly journals Klotho Deficiency Accelerates Stem Cells Aging by Impairing Telomerase Activity

2018 ◽  
Vol 74 (9) ◽  
pp. 1396-1407 ◽  
Author(s):  
Mujib Ullah ◽  
Zhongjie Sun
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Critical Role ◽  
Telomerase Activity ◽  
Cell Aging ◽  
Treated Animal ◽  
Differentiation Potential ◽  
Telomere Shortening ◽  
Altered Expression ◽  
Stem Cell Aging

Abstract Understanding the effect of molecular pathways involved in the age-dependent deterioration of stem cell function is critical for developing new therapies. The overexpression of Klotho (KL), an antiaging protein, causes treated animal models to enjoy extended life spans. Now, the question stands: Does KL deficiency accelerate stem cell aging and telomere shortening? If so, what are the specific mechanisms by which it does this, and is cycloastragenol (CAG) treatment enough to restore telomerase activity in aged stem cells? We found that KL deficiency diminished telomerase activity by altering the expression of TERF1 and TERT, causing impaired differentiation potential, pluripotency, cellular senescence, and apoptosis in stem cells. Telomerase activity decreased with KL-siRNA knockdown. This suggests that both KL and telomeres regulate the stem cell aging process through telomerase subunits TERF1, POT1, and TERT using the TGFβ, Insulin, and Wnt signaling. These pathways can rejuvenate stem cell populations in a CD90-dependent mechanism. Stem cell dysfunctions were largely provoked by KL deficiency and telomere shortening, owing to altered expression of TERF1, TGFβ1, CD90, POT1, TERT, and basic fibroblast growth factor (bFGF). The CAG treatment partially rescued telomerase deterioration, suggesting that KL plays a critical role in life-extension by regulating telomere length and telomerase activity.

scholarly journals Aging of hematopoietic stem cells

Blood ◽  
2018 ◽  
Vol 131 (5) ◽  
pp. 479-487 ◽  
Author(s):  
Gerald de Haan ◽  
Seka Simone Lazare
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Hematopoietic Stem Cells ◽  
Blood Cells ◽  
Aging Process ◽  
Molecular Mechanisms ◽  
Cell Aging ◽  
Self Renewal ◽  
Hematopoietic Stem ◽  
Stem Cell Aging

Abstract Hematopoietic stem cells (HSCs) ensure a balanced production of all blood cells throughout life. As they age, HSCs gradually lose their self-renewal and regenerative potential, whereas the occurrence of cellular derailment strongly increases. Here we review our current understanding of the molecular mechanisms that contribute to HSC aging. We argue that most of the causes that underlie HSC aging result from cell-intrinsic pathways, and reflect on which aspects of the aging process may be reversible. Because many hematological pathologies are strongly age-associated, strategies to intervene in aspects of the stem cell aging process may have significant clinical relevance.

Serine Metabolism Controls Dental Pulp Stem Cell Aging by Regulating the DNA Methylation of p16

2020 ◽  
Vol 100 (1) ◽  
pp. 90-97
Author(s):  
R.L. Yang ◽  
H.M. Huang ◽  
C.S. Han ◽  
S.J. Cui ◽  
Y.K. Zhou ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Stem Cells ◽  
Stem Cell ◽  
Dental Pulp ◽  
Permanent Teeth ◽  
Deciduous Teeth ◽  
Cell Aging ◽  
Differentiation Capacity ◽  
Stem Cell Aging ◽  
Serine Metabolism

To investigate the characteristics and molecular events of dental pulp stem cells (DPSCs) for tissue regeneration with aging, we isolated and analyzed the stem cells from human exfoliated deciduous teeth (SHED) and permanent teeth of young (Y-DPSCs) and old (A-DPSCs) adults. Results showed that the stemness and osteogenic differentiation capacity of DPSCs decreased with aging. The RNA sequencing results showed that glycine, serine, and threonine metabolism was one of the most enriched gene clusters among SHED, Y-DPSCs, and A-DPSCs, according to analysis based on the Kyoto Encyclopedia of Genes and Genomes. The expression of serine metabolism–related enzymes phosphoserine aminotransferase 1 (PSAT1) and phosphoglycerate (PHGDH) decreased in A-DPSCs and provided less methyl donor S-adenosylmethionine (SAM) for DNA methylation, leading to the hypomethylation of the senescence marker p16 (CDNK2A). Furthermore, the proliferation and differentiation capacity of Y-DPSCs and SHED decreased after PHGDH siRNA treatment, which reduced the level of SAM. Convincingly, the ratios of PSAT1-, PHGDH-, or proliferating cell nuclear antigen–positive cells in the dental pulp of old permanent teeth were less than those in the dental pulp of deciduous teeth and young permanent teeth. In summary, the stemness and differentiation capacity of DPSCs decreased with aging. The decreased serine metabolism in A-DPSCs upregulated the expression of p16 via attenuating its DNA methylation, resulting in DPSC aging. Our finding indicated that serine metabolism and 1 carbon unit participated in stem cell aging, which provided new direction for stem cell aging study and intervention.

Caloric restriction maintains stem cells through niche and regulates stem cell aging

2019 ◽  
Vol 98 (1) ◽  
pp. 25-37 ◽  
Author(s):  
Nagarajan Maharajan ◽  
Karthikeyan Vijayakumar ◽  
Chul Ho Jang ◽  
Goang-Won Cho
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Caloric Restriction ◽  
Cell Aging ◽  
Stem Cell Aging

scholarly journals Investigation of Stem Cell Aging Throughout the Lifetime and Therapeutic Opportunities

2020 ◽  
Author(s):  
Sarah Karimi ◽  
Setareh Raoufi ◽  
Zohreh Bagher
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Aging Process ◽  
Cell Function ◽  
Cell Activity ◽  
The Body ◽  
Natural Phenomenon ◽  
Cell Aging ◽  
Molecular Pathways ◽  
Stem Cell Aging

Introduction: Aging is a natural phenomenon that is caused by changes in the cells of the body. Theoretically, aging starts from birth and lasts throughout life. These changes affect the function of the cells. Also, in old tissues, the capacity for homeostasis and tissue repair is decline due to destructive changes in specific tissue stem cells, niche of stem cells and systemic factors that regulate stem cell activity. Understanding molecular pathways that disrupt stem cell function during aging is crucial for the development of new treatments for aging-associated diseases. In this article, the symptoms of stem cell aging and the key molecular pathways that are commonly used for the aging of stem cells were discussed. We will consider experimental evidence for all of the mechanisms and evaluate the way that can slow down or even stop the aging process. Finally, we will look at the aging process of three types of stem cells.

New insights into skin stem cell aging and cancer

2014 ◽  
Vol 42 (3) ◽  
pp. 663-669 ◽  
Author(s):  
M. Carmen Ortells ◽  
William M. Keyes
Keyword(s):  
Stem Cells ◽  
Molecular Mechanisms ◽  
Cell Aging ◽  
Adult Tissue ◽  
Self Renewal ◽  
Tissue Specific ◽  
Regulatory Processes ◽  
Age Related ◽  
Stem Cell Aging ◽  
Growth Properties

Adult tissue homoeostasis requires continual replacement of cells that are lost due to normal turnover, injury and disease. However, aging is associated with an overall decline in tissue function and homoeostasis, suggesting that the normal regulatory processes that govern self-renewal and regeneration may become impaired with age. Tissue-specific SCs (stem cells) lie at the apex of organismal conservation and regeneration, ultimately being responsible for continued tissue maintenance. In many tissues, there are changes in SC numbers, or alteration of their growth properties during aging, often involving imbalances in tumour-suppressor- and oncogene-mediated pathways. Uncovering the molecular mechanisms leading to changes in SC function during aging will provide an essential tool to address tissue-specific age-related pathologies. In the present review, we summarize the age-related alterations found in different tissue SC populations, highlighting recently identified changes in aged HFSCs (hair-follicle SCs) in the skin.

scholarly journals Manifestations and mechanisms of stem cell aging

2011 ◽  
Vol 193 (2) ◽  
pp. 257-266 ◽  
Author(s):  
Ling Liu ◽  
Thomas A. Rando
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Adult Stem Cells ◽  
Cell Aging ◽  
Functional Changes ◽  
Cell Based Therapy ◽  
Age Related ◽  
Stem Cell Aging ◽  
Genetic Interventions ◽  
Cell Functionality

Adult stem cells exist in most mammalian organs and tissues and are indispensable for normal tissue homeostasis and repair. In most tissues, there is an age-related decline in stem cell functionality but not a depletion of stem cells. Such functional changes reflect deleterious effects of age on the genome, epigenome, and proteome, some of which arise cell autonomously and others of which are imposed by an age-related change in the local milieu or systemic environment. Notably, some of the changes, particularly epigenomic and proteomic, are potentially reversible, and both environmental and genetic interventions can result in the rejuvenation of aged stem cells. Such findings have profound implications for the stem cell–based therapy of age-related diseases.

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