Cellular Senescence in Type 2 Diabetes: A Therapeutic Opportunity

Cellular senescence is a fundamental aging mechanism that has been implicated in many age-related diseases and is a significant cause of tissue dysfunction. Accumulation of senescent cells occurs during aging and is also seen in the context of obesity and diabetes. Senescent cells may play a role in...

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Published in	Diabetes (New York, N.Y.) Vol. 64; no. 7; pp. 2289 - 2298
Main Authors	Palmer, Allyson K., Tchkonia, Tamara, LeBrasseur, Nathan K., Chini, Eduardo N., Xu, Ming, Kirkland, James L.
Format	Journal Article
Language	English
Published	United States American Diabetes Association 01.07.2015
Subjects	Adipose Tissue - physiology Aging Animals Cells Cellular Microenvironment Cellular Senescence Ceramides - metabolism Diabetes Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - etiology Diabetes Mellitus, Type 2 - pathology Diabetes Mellitus, Type 2 - therapy Humans Insulin Resistance Insulin-Like Growth Factor Binding Protein 3 - physiology Insulin-Like Growth Factor I - physiology Insulin-Secreting Cells - pathology Obesity Pathogenesis s in Diabetes Tissues
Online Access	Get full text
ISSN	0012-1797 1939-327X 1939-327X
DOI	10.2337/db14-1820

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Abstract	Cellular senescence is a fundamental aging mechanism that has been implicated in many age-related diseases and is a significant cause of tissue dysfunction. Accumulation of senescent cells occurs during aging and is also seen in the context of obesity and diabetes. Senescent cells may play a role in type 2 diabetes pathogenesis through direct impact on pancreatic β-cell function, senescence-associated secretory phenotype (SASP)-mediated tissue damage, and involvement in adipose tissue dysfunction. In turn, metabolic and signaling changes seen in diabetes, such as high circulating glucose, altered lipid metabolism, and growth hormone axis perturbations, can promote senescent cell formation. Thus, senescent cells might be part of a pathogenic loop in diabetes, as both a cause and consequence of metabolic changes and tissue damage. Therapeutic targeting of a basic aging mechanism such as cellular senescence may have a large impact on disease pathogenesis and could be more effective in preventing the progression of diabetes complications than currently available therapies that have limited impact on already existing tissue damage. Therefore, senescent cells and the SASP represent significant opportunities for advancement in the prevention and treatment of type 2 diabetes and its complications.
AbstractList	Cellular senescence is a fundamental aging mechanism that has been implicated in many age-related diseases and is a significant cause of tissue dysfunction. Accumulation of senescent cells occurs during aging and is also seen in the context of obesity and diabetes. Senescent cells may play a role in type 2 diabetes pathogenesis through direct impact on pancreatic β-cell function, senescence-associated secretory phenotype (SASP)-mediated tissue damage, and involvement in adipose tissue dysfunction. In turn, metabolic and signaling changes seen in diabetes, such as high circulating glucose, altered lipid metabolism, and growth hormone axis perturbations, can promote senescent cell formation. Thus, senescent cells might be part of a pathogenic loop in diabetes, as both a cause and consequence of metabolic changes and tissue damage. Therapeutic targeting of a basic aging mechanism such as cellular senescence may have a large impact on disease pathogenesis and could be more effective in preventing the progression of diabetes complications than currently available therapies that have limited impact on already existing tissue damage. Therefore, senescent cells and the SASP represent significant opportunities for advancement in the prevention and treatment of type 2 diabetes and its complications. Cellular senescence is a fundamental aging mechanism that has been implicated in many age-related diseases and is a significant cause of tissue dysfunction. Accumulation of senescent cells occurs during aging and is also seen in the context of obesity and diabetes. Senescent cells may play a role in type 2 diabetes pathogenesis through direct impact on pancreatic β-cell function, senescence-associated secretory phenotype (SASP)-mediated tissue damage, and involvement in adipose tissue dysfunction. In turn, metabolic and signaling changes seen in diabetes, such as high circulating glucose, altered lipid metabolism, and growth hormone axis perturbations, can promote senescent cell formation. Thus, senescent cells might be part of a pathogenic loop in diabetes, as both a cause and consequence of metabolic changes and tissue damage. Therapeutic targeting of a basic aging mechanism such as cellular senescence may have a large impact on disease pathogenesis and could be more effective in preventing the progression of diabetes complications than currently available therapies that have limited impact on already existing tissue damage. Therefore, senescent cells and the SASP represent significant opportunities for advancement in the prevention and treatment of type 2 diabetes and its complications.Cellular senescence is a fundamental aging mechanism that has been implicated in many age-related diseases and is a significant cause of tissue dysfunction. Accumulation of senescent cells occurs during aging and is also seen in the context of obesity and diabetes. Senescent cells may play a role in type 2 diabetes pathogenesis through direct impact on pancreatic β-cell function, senescence-associated secretory phenotype (SASP)-mediated tissue damage, and involvement in adipose tissue dysfunction. In turn, metabolic and signaling changes seen in diabetes, such as high circulating glucose, altered lipid metabolism, and growth hormone axis perturbations, can promote senescent cell formation. Thus, senescent cells might be part of a pathogenic loop in diabetes, as both a cause and consequence of metabolic changes and tissue damage. Therapeutic targeting of a basic aging mechanism such as cellular senescence may have a large impact on disease pathogenesis and could be more effective in preventing the progression of diabetes complications than currently available therapies that have limited impact on already existing tissue damage. Therefore, senescent cells and the SASP represent significant opportunities for advancement in the prevention and treatment of type 2 diabetes and its complications.
Author	Chini, Eduardo N. Xu, Ming Tchkonia, Tamara LeBrasseur, Nathan K. Kirkland, James L. Palmer, Allyson K.
Author_xml	– sequence: 1 givenname: Allyson K. surname: Palmer fullname: Palmer, Allyson K. organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, Mayo Medical Scientist Training Program, Mayo Graduate School, Mayo Medical School, Rochester, MN – sequence: 2 givenname: Tamara surname: Tchkonia fullname: Tchkonia, Tamara organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN – sequence: 3 givenname: Nathan K. surname: LeBrasseur fullname: LeBrasseur, Nathan K. organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN – sequence: 4 givenname: Eduardo N. surname: Chini fullname: Chini, Eduardo N. organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, Department of Anesthesiology, Mayo Clinic, Rochester, MN – sequence: 5 givenname: Ming surname: Xu fullname: Xu, Ming organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN – sequence: 6 givenname: James L. surname: Kirkland fullname: Kirkland, James L. organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/26106186$$D View this record in MEDLINE/PubMed
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Copyright	2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. Copyright American Diabetes Association Jul 2015 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. 2015
Copyright_xml	– notice: 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. – notice: Copyright American Diabetes Association Jul 2015 – notice: 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. 2015
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Snippet	Cellular senescence is a fundamental aging mechanism that has been implicated in many age-related diseases and is a significant cause of tissue dysfunction....
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SubjectTerms	Adipose Tissue - physiology Aging Animals Cells Cellular Microenvironment Cellular Senescence Ceramides - metabolism Diabetes Diabetes Mellitus, Type 2 - complications Diabetes Mellitus, Type 2 - etiology Diabetes Mellitus, Type 2 - pathology Diabetes Mellitus, Type 2 - therapy Humans Insulin Resistance Insulin-Like Growth Factor Binding Protein 3 - physiology Insulin-Like Growth Factor I - physiology Insulin-Secreting Cells - pathology Obesity Pathogenesis s in Diabetes Tissues
Title	Cellular Senescence in Type 2 Diabetes: A Therapeutic Opportunity
URI	https://www.ncbi.nlm.nih.gov/pubmed/26106186 https://www.proquest.com/docview/1693697907 https://www.proquest.com/docview/1691287122 https://pubmed.ncbi.nlm.nih.gov/PMC4477358
Volume	64
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