Fisetin is a senotherapeutic that extends health and lifespan
Senescence is a tumor suppressor mechanism activated in stressed cells to prevent replication of damaged DNA. Senescent cells have been demonstrated to play a causal role in driving aging and age-related diseases using genetic and pharmacologic approaches. We previously demonstrated that the combina...
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| Vydané v: | EBioMedicine Ročník 36; s. 18 - 28 |
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| Hlavní autori: | , , , , , , , , , , , , , , , , , , , , , |
| Médium: | Journal Article |
| Jazyk: | English |
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Netherlands
Elsevier B.V
01.10.2018
Elsevier |
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| ISSN: | 2352-3964, 2352-3964 |
| On-line prístup: | Získať plný text |
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| Abstract | Senescence is a tumor suppressor mechanism activated in stressed cells to prevent replication of damaged DNA. Senescent cells have been demonstrated to play a causal role in driving aging and age-related diseases using genetic and pharmacologic approaches. We previously demonstrated that the combination of dasatinib and the flavonoid quercetin is a potent senolytic improving numerous age-related conditions including frailty, osteoporosis and cardiovascular disease. The goal of this study was to identify flavonoids with more potent senolytic activity.
A panel of flavonoid polyphenols was screened for senolytic activity using senescent murine and human fibroblasts, driven by oxidative and genotoxic stress, respectively. The top senotherapeutic flavonoid was tested in mice modeling a progeroid syndrome carrying a p16INK4a-luciferase reporter and aged wild-type mice to determine the effects of fisetin on senescence markers, age-related histopathology, disease markers, health span and lifespan. Human adipose tissue explants were used to determine if results translated.
Of the 10 flavonoids tested, fisetin was the most potent senolytic. Acute or intermittent treatment of progeroid and old mice with fisetin reduced senescence markers in multiple tissues, consistent with a hit-and-run senolytic mechanism. Fisetin reduced senescence in a subset of cells in murine and human adipose tissue, demonstrating cell-type specificity. Administration of fisetin to wild-type mice late in life restored tissue homeostasis, reduced age-related pathology, and extended median and maximum lifespan.
The natural product fisetin has senotherapeutic activity in mice and in human tissues. Late life intervention was sufficient to yield a potent health benefit. These characteristics suggest the feasibility to translation to human clinical studies.
NIH grants P01 AG043376 (PDR, LJN), U19 AG056278 (PDR, LJN, WLL), R24 AG047115 (WLL), R37 AG013925 (JLK), R21 AG047984 (JLK), P30 DK050456 (Adipocyte Subcore, JLK), a Glenn Foundation/American Federation for Aging Research (AFAR) BIG Award (JLK), Glenn/AFAR (LJN, CEB), the Ted Nash Long Life and Noaber Foundations (JLK), the Connor Group (JLK), Robert J. and Theresa W. Ryan (JLK), and a Minnesota Partnership Grant (AMAY-UMN#99)-P004610401–1 (JLK, EAA). |
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| AbstractList | Senescence is a tumor suppressor mechanism activated in stressed cells to prevent replication of damaged DNA. Senescent cells have been demonstrated to play a causal role in driving aging and age-related diseases using genetic and pharmacologic approaches. We previously demonstrated that the combination of dasatinib and the flavonoid quercetin is a potent senolytic improving numerous age-related conditions including frailty, osteoporosis and cardiovascular disease. The goal of this study was to identify flavonoids with more potent senolytic activity.
A panel of flavonoid polyphenols was screened for senolytic activity using senescent murine and human fibroblasts, driven by oxidative and genotoxic stress, respectively. The top senotherapeutic flavonoid was tested in mice modeling a progeroid syndrome carrying a p16INK4a-luciferase reporter and aged wild-type mice to determine the effects of fisetin on senescence markers, age-related histopathology, disease markers, health span and lifespan. Human adipose tissue explants were used to determine if results translated.
Of the 10 flavonoids tested, fisetin was the most potent senolytic. Acute or intermittent treatment of progeroid and old mice with fisetin reduced senescence markers in multiple tissues, consistent with a hit-and-run senolytic mechanism. Fisetin reduced senescence in a subset of cells in murine and human adipose tissue, demonstrating cell-type specificity. Administration of fisetin to wild-type mice late in life restored tissue homeostasis, reduced age-related pathology, and extended median and maximum lifespan.
The natural product fisetin has senotherapeutic activity in mice and in human tissues. Late life intervention was sufficient to yield a potent health benefit. These characteristics suggest the feasibility to translation to human clinical studies.
NIH grants P01 AG043376 (PDR, LJN), U19 AG056278 (PDR, LJN, WLL), R24 AG047115 (WLL), R37 AG013925 (JLK), R21 AG047984 (JLK), P30 DK050456 (Adipocyte Subcore, JLK), a Glenn Foundation/American Federation for Aging Research (AFAR) BIG Award (JLK), Glenn/AFAR (LJN, CEB), the Ted Nash Long Life and Noaber Foundations (JLK), the Connor Group (JLK), Robert J. and Theresa W. Ryan (JLK), and a Minnesota Partnership Grant (AMAY-UMN#99)-P004610401–1 (JLK, EAA). Senescence is a tumor suppressor mechanism activated in stressed cells to prevent replication of damaged DNA. Senescent cells have been demonstrated to play a causal role in driving aging and age-related diseases using genetic and pharmacologic approaches. We previously demonstrated that the combination of dasatinib and the flavonoid quercetin is a potent senolytic improving numerous age-related conditions including frailty, osteoporosis and cardiovascular disease. The goal of this study was to identify flavonoids with more potent senolytic activity. A panel of flavonoid polyphenols was screened for senolytic activity using senescent murine and human fibroblasts, driven by oxidative and genotoxic stress, respectively. The top senotherapeutic flavonoid was tested in mice modeling a progeroid syndrome carrying a p16 -luciferase reporter and aged wild-type mice to determine the effects of fisetin on senescence markers, age-related histopathology, disease markers, health span and lifespan. Human adipose tissue explants were used to determine if results translated. Of the 10 flavonoids tested, fisetin was the most potent senolytic. Acute or intermittent treatment of progeroid and old mice with fisetin reduced senescence markers in multiple tissues, consistent with a hit-and-run senolytic mechanism. Fisetin reduced senescence in a subset of cells in murine and human adipose tissue, demonstrating cell-type specificity. Administration of fisetin to wild-type mice late in life restored tissue homeostasis, reduced age-related pathology, and extended median and maximum lifespan. The natural product fisetin has senotherapeutic activity in mice and in human tissues. Late life intervention was sufficient to yield a potent health benefit. These characteristics suggest the feasibility to translation to human clinical studies. FUND: NIH grants P01 AG043376 (PDR, LJN), U19 AG056278 (PDR, LJN, WLL), R24 AG047115 (WLL), R37 AG013925 (JLK), R21 AG047984 (JLK), P30 DK050456 (Adipocyte Subcore, JLK), a Glenn Foundation/American Federation for Aging Research (AFAR) BIG Award (JLK), Glenn/AFAR (LJN, CEB), the Ted Nash Long Life and Noaber Foundations (JLK), the Connor Group (JLK), Robert J. and Theresa W. Ryan (JLK), and a Minnesota Partnership Grant (AMAY-UMN#99)-P004610401-1 (JLK, EAA). AbstractBackgroundSenescence is a tumor suppressor mechanism activated in stressed cells to prevent replication of damaged DNA. Senescent cells have been demonstrated to play a causal role in driving aging and age-related diseases using genetic and pharmacologic approaches. We previously demonstrated that the combination of dasatinib and the flavonoid quercetin is a potent senolytic improving numerous age-related conditions including frailty, osteoporosis and cardiovascular disease. The goal of this study was to identify flavonoids with more potent senolytic activity. MethodsA panel of flavonoid polyphenols was screened for senolytic activity using senescent murine and human fibroblasts, driven by oxidative and genotoxic stress, respectively. The top senotherapeutic flavonoid was tested in mice modeling a progeroid syndrome carrying a p16 INK4a-luciferase reporter and aged wild-type mice to determine the effects of fisetin on senescence markers, age-related histopathology, disease markers, health span and lifespan. Human adipose tissue explants were used to determine if results translated. FindingsOf the 10 flavonoids tested, fisetin was the most potent senolytic. Acute or intermittent treatment of progeroid and old mice with fisetin reduced senescence markers in multiple tissues, consistent with a hit-and-run senolytic mechanism. Fisetin reduced senescence in a subset of cells in murine and human adipose tissue, demonstrating cell-type specificity. Administration of fisetin to wild-type mice late in life restored tissue homeostasis, reduced age-related pathology, and extended median and maximum lifespan. InterpretationThe natural product fisetin has senotherapeutic activity in mice and in human tissues. Late life intervention was sufficient to yield a potent health benefit. These characteristics suggest the feasibility to translation to human clinical studies. FundNIH grants P01 AG043376 (PDR, LJN), U19 AG056278 (PDR, LJN, WLL), R24 AG047115 (WLL), R37 AG013925 (JLK), R21 AG047984 (JLK), P30 DK050456 (Adipocyte Subcore, JLK), a Glenn Foundation/ American Federation for Aging Research (AFAR) BIG Award (JLK), Glenn/AFAR (LJN, CEB), the Ted Nash Long Life and Noaber Foundations (JLK), the Connor Group (JLK), Robert J. and Theresa W. Ryan (JLK), and a Minnesota Partnership Grant (AMAY-UMN#99)-P004610401–1 (JLK, EAA). Senescence is a tumor suppressor mechanism activated in stressed cells to prevent replication of damaged DNA. Senescent cells have been demonstrated to play a causal role in driving aging and age-related diseases using genetic and pharmacologic approaches. We previously demonstrated that the combination of dasatinib and the flavonoid quercetin is a potent senolytic improving numerous age-related conditions including frailty, osteoporosis and cardiovascular disease. The goal of this study was to identify flavonoids with more potent senolytic activity.BACKGROUNDSenescence is a tumor suppressor mechanism activated in stressed cells to prevent replication of damaged DNA. Senescent cells have been demonstrated to play a causal role in driving aging and age-related diseases using genetic and pharmacologic approaches. We previously demonstrated that the combination of dasatinib and the flavonoid quercetin is a potent senolytic improving numerous age-related conditions including frailty, osteoporosis and cardiovascular disease. The goal of this study was to identify flavonoids with more potent senolytic activity.A panel of flavonoid polyphenols was screened for senolytic activity using senescent murine and human fibroblasts, driven by oxidative and genotoxic stress, respectively. The top senotherapeutic flavonoid was tested in mice modeling a progeroid syndrome carrying a p16INK4a-luciferase reporter and aged wild-type mice to determine the effects of fisetin on senescence markers, age-related histopathology, disease markers, health span and lifespan. Human adipose tissue explants were used to determine if results translated.METHODSA panel of flavonoid polyphenols was screened for senolytic activity using senescent murine and human fibroblasts, driven by oxidative and genotoxic stress, respectively. The top senotherapeutic flavonoid was tested in mice modeling a progeroid syndrome carrying a p16INK4a-luciferase reporter and aged wild-type mice to determine the effects of fisetin on senescence markers, age-related histopathology, disease markers, health span and lifespan. Human adipose tissue explants were used to determine if results translated.Of the 10 flavonoids tested, fisetin was the most potent senolytic. Acute or intermittent treatment of progeroid and old mice with fisetin reduced senescence markers in multiple tissues, consistent with a hit-and-run senolytic mechanism. Fisetin reduced senescence in a subset of cells in murine and human adipose tissue, demonstrating cell-type specificity. Administration of fisetin to wild-type mice late in life restored tissue homeostasis, reduced age-related pathology, and extended median and maximum lifespan.FINDINGSOf the 10 flavonoids tested, fisetin was the most potent senolytic. Acute or intermittent treatment of progeroid and old mice with fisetin reduced senescence markers in multiple tissues, consistent with a hit-and-run senolytic mechanism. Fisetin reduced senescence in a subset of cells in murine and human adipose tissue, demonstrating cell-type specificity. Administration of fisetin to wild-type mice late in life restored tissue homeostasis, reduced age-related pathology, and extended median and maximum lifespan.The natural product fisetin has senotherapeutic activity in mice and in human tissues. Late life intervention was sufficient to yield a potent health benefit. These characteristics suggest the feasibility to translation to human clinical studies. FUND: NIH grants P01 AG043376 (PDR, LJN), U19 AG056278 (PDR, LJN, WLL), R24 AG047115 (WLL), R37 AG013925 (JLK), R21 AG047984 (JLK), P30 DK050456 (Adipocyte Subcore, JLK), a Glenn Foundation/American Federation for Aging Research (AFAR) BIG Award (JLK), Glenn/AFAR (LJN, CEB), the Ted Nash Long Life and Noaber Foundations (JLK), the Connor Group (JLK), Robert J. and Theresa W. Ryan (JLK), and a Minnesota Partnership Grant (AMAY-UMN#99)-P004610401-1 (JLK, EAA).INTERPRETATIONThe natural product fisetin has senotherapeutic activity in mice and in human tissues. Late life intervention was sufficient to yield a potent health benefit. These characteristics suggest the feasibility to translation to human clinical studies. FUND: NIH grants P01 AG043376 (PDR, LJN), U19 AG056278 (PDR, LJN, WLL), R24 AG047115 (WLL), R37 AG013925 (JLK), R21 AG047984 (JLK), P30 DK050456 (Adipocyte Subcore, JLK), a Glenn Foundation/American Federation for Aging Research (AFAR) BIG Award (JLK), Glenn/AFAR (LJN, CEB), the Ted Nash Long Life and Noaber Foundations (JLK), the Connor Group (JLK), Robert J. and Theresa W. Ryan (JLK), and a Minnesota Partnership Grant (AMAY-UMN#99)-P004610401-1 (JLK, EAA). |
| Author | Ladiges, Warren L. Wade, Erin A. McGuckian, Collin Tchkonia, Tamara Zhu, Yi Ling, Yuan Yuan Yousefzadeh, Matthew J. Fuhrmann-Stroissnigg, Heike Burd, Christin E. Kirkland, James L. Grassi, Diego McGowan, Sara J. Wentworth, Mark Robbins, Paul D. Kato, Jonathon I. Pirtskhalava, Tamar Angelini, Luise Xu, Ming Melos, Kendra I. Arriaga, Edgar A. Niedernhofer, Laura J. Inman, Christina L. |
| AuthorAffiliation | c Office of Research Regulatory Support, Mayo Clinic, Rochester, MN 55905, United States a Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States f Department of Comparative Medicine, University of Washington, Seattle, WA 98195, United States b Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First St., S.W., Rochester, MN 55905, United States e Department of Chemistry, University of Minnesota, Minneapolis, MN 55455-0431, United States d Department of Molecular Genetics and Cancer Biology and Genetics, The Ohio State University, Columbus, OH 43210, United States |
| AuthorAffiliation_xml | – name: d Department of Molecular Genetics and Cancer Biology and Genetics, The Ohio State University, Columbus, OH 43210, United States – name: c Office of Research Regulatory Support, Mayo Clinic, Rochester, MN 55905, United States – name: e Department of Chemistry, University of Minnesota, Minneapolis, MN 55455-0431, United States – name: f Department of Comparative Medicine, University of Washington, Seattle, WA 98195, United States – name: b Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First St., S.W., Rochester, MN 55905, United States – name: a Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States |
| Author_xml | – sequence: 1 givenname: Matthew J. surname: Yousefzadeh fullname: Yousefzadeh, Matthew J. organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 2 givenname: Yi surname: Zhu fullname: Zhu, Yi organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First St., S.W., Rochester, MN 55905, United States – sequence: 3 givenname: Sara J. surname: McGowan fullname: McGowan, Sara J. organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 4 givenname: Luise surname: Angelini fullname: Angelini, Luise organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 5 givenname: Heike surname: Fuhrmann-Stroissnigg fullname: Fuhrmann-Stroissnigg, Heike organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 6 givenname: Ming surname: Xu fullname: Xu, Ming organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First St., S.W., Rochester, MN 55905, United States – sequence: 7 givenname: Yuan Yuan surname: Ling fullname: Ling, Yuan Yuan organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 8 givenname: Kendra I. surname: Melos fullname: Melos, Kendra I. organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 9 givenname: Tamar surname: Pirtskhalava fullname: Pirtskhalava, Tamar organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First St., S.W., Rochester, MN 55905, United States – sequence: 10 givenname: Christina L. surname: Inman fullname: Inman, Christina L. organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First St., S.W., Rochester, MN 55905, United States – sequence: 11 givenname: Collin surname: McGuckian fullname: McGuckian, Collin organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 12 givenname: Erin A. surname: Wade fullname: Wade, Erin A. organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 13 givenname: Jonathon I. surname: Kato fullname: Kato, Jonathon I. organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 14 givenname: Diego surname: Grassi fullname: Grassi, Diego organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 15 givenname: Mark surname: Wentworth fullname: Wentworth, Mark organization: Office of Research Regulatory Support, Mayo Clinic, Rochester, MN 55905, United States – sequence: 16 givenname: Christin E. surname: Burd fullname: Burd, Christin E. organization: Department of Molecular Genetics and Cancer Biology and Genetics, The Ohio State University, Columbus, OH 43210, United States – sequence: 17 givenname: Edgar A. surname: Arriaga fullname: Arriaga, Edgar A. organization: Department of Chemistry, University of Minnesota, Minneapolis, MN 55455-0431, United States – sequence: 18 givenname: Warren L. surname: Ladiges fullname: Ladiges, Warren L. organization: Department of Comparative Medicine, University of Washington, Seattle, WA 98195, United States – sequence: 19 givenname: Tamara surname: Tchkonia fullname: Tchkonia, Tamara organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First St., S.W., Rochester, MN 55905, United States – sequence: 20 givenname: James L. surname: Kirkland fullname: Kirkland, James L. organization: Robert and Arlene Kogod Center on Aging, Mayo Clinic, 200 First St., S.W., Rochester, MN 55905, United States – sequence: 21 givenname: Paul D. surname: Robbins fullname: Robbins, Paul D. email: probbins@umn.edu organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States – sequence: 22 givenname: Laura J. surname: Niedernhofer fullname: Niedernhofer, Laura J. email: lniedern@umn.edu organization: Department of Molecular Medicine and the Center on Aging, The Scripps Research Institute, 130 Scripps Way, Jupiter, FL 33458, United States |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30279143$$D View this record in MEDLINE/PubMed |
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| Snippet | Senescence is a tumor suppressor mechanism activated in stressed cells to prevent replication of damaged DNA. Senescent cells have been demonstrated to play a... AbstractBackgroundSenescence is a tumor suppressor mechanism activated in stressed cells to prevent replication of damaged DNA. Senescent cells have been... |
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| SubjectTerms | Adipose Tissue - metabolism Advanced Basic Science Aging Animals Biological Products - pharmacology Biological Products - therapeutic use Biomarkers Cellular Senescence - drug effects Cellular Senescence - genetics Female Fibroblasts - drug effects Fibroblasts - metabolism Flavonoids - pharmacology Flavonoids - therapeutic use Flavonols Gene Expression Genes, Reporter Health Status Healthspan Humans Internal Medicine Lifespan Lipid Peroxidation Longevity - drug effects Male Mice Mice, Knockout Progeria Research paper Senescence Senolytic |
| Title | Fisetin is a senotherapeutic that extends health and lifespan |
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