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Artikel ; Online: Senescence markers in subcutaneous preadipocytes differ in childhood- versus adult-onset obesity before and after weight loss.

Murphy, Jessica / Tam, Bjorn T / Kirkland, James L / Tchkonia, Tamara / Giorgadze, Nino / Pirtskhalava, Tamar / Tsoukas, Michael A / Morais, José A / Santosa, Sylvia

Obesity (Silver Spring, Md.)

2023 Band 31, Heft 6, Seite(n) 1610–1619

Abstract: Objective: The aim of this study was to determine the effect of age of obesity onset on senescence-related markers in abdominal (AB) and femoral (FEM) subcutaneous adipose tissue (SAT) before and after moderate (~10%) weight loss.: Methods: AB and ... ...

Abstract	Objective: The aim of this study was to determine the effect of age of obesity onset on senescence-related markers in abdominal (AB) and femoral (FEM) subcutaneous adipose tissue (SAT) before and after moderate (~10%) weight loss. Methods: AB and FEM SAT were collected from human females with childhood-onset obesity (CO) or adult-onset obesity (AO) before and after diet- and exercise-induced weight loss. Immunofluorescence analysis of γH2AX/RAD51 (DNA damage/repair markers) and p53/p21 (senescence markers) was conducted in cultured preadipocytes, and senescence-associated β-galactosidase (SA-β-gal) activity was measured in SAT. Results: CO had proportionately more AB and FEM preadipocytes with DNA damage (γH2AX Conclusions: These results provide preliminary evidence that females with CO have an accelerated preadipocyte aging state that improves with weight loss in terms of DNA damage but not senescence.
Mesh-Begriff(e)	Female ; Humans ; Adult ; Cellular Senescence ; Tumor Suppressor Protein p53/pharmacology ; Aging ; Obesity ; Subcutaneous Fat
Chemische Substanzen	Tumor Suppressor Protein p53
Sprache	Englisch
Erscheinungsdatum	2023-05-17
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2230457-5
ISSN	1930-739X ; 1071-7323 ; 1930-7381
ISSN (online)	1930-739X
ISSN	1071-7323 ; 1930-7381
DOI	10.1002/oby.23745
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: A chronic wound model to investigate skin cellular senescence.

Wyles, Saranya P / Dashti, Parisa / Pirtskhalava, Tamar / Tekin, Burak / Inman, Christina / Gomez, Lilian Sales / Lagnado, Anthony B / Prata, Larissa / Jurk, Diana / Passos, João F / Tchkonia, Tamar / Kirkland, James L

Aging

2023 Band 15, Heft 8, Seite(n) 2852–2862

Abstract: Wound healing is an essential physiological process for restoring normal skin structure and function post-injury. The role of cellular senescence, an essentially irreversible cell cycle state in response to damaging stimuli, has emerged as a critical ... ...

Abstract	Wound healing is an essential physiological process for restoring normal skin structure and function post-injury. The role of cellular senescence, an essentially irreversible cell cycle state in response to damaging stimuli, has emerged as a critical mechanism in wound remodeling. Transiently-induced senescence during tissue remodeling has been shown to be beneficial in the acute wound healing phase. In contrast, persistent senescence, as observed in chronic wounds, contributes to delayed closure. Herein we describe a chronic wound murine model and its cellular senescence profile, including the senescence-associated secretory phenotype.
Mesh-Begriff(e)	Mice ; Animals ; Cellular Senescence/physiology ; Skin/metabolism ; Wound Healing/physiology ; Cell Division ; Senescence-Associated Secretory Phenotype
Sprache	Englisch
Erscheinungsdatum	2023-04-21
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.204667
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Profiling microRNA expression during senescence and aging: mining for a diagnostic tool of senescent-cell burden.

bioRxiv : the preprint server for biology

2024

Abstract: In the last decade cellular senescence, a hallmark of aging, has come into focus for pharmacologically targeting aging processes. Senolytics are one of these interventive strategies that have advanced into clinical trials, creating an unmet need for ... ...

Abstract	In the last decade cellular senescence, a hallmark of aging, has come into focus for pharmacologically targeting aging processes. Senolytics are one of these interventive strategies that have advanced into clinical trials, creating an unmet need for minimally invasive biomarkers of senescent cell load to identify patients at need for senotherapy. We created a landscape of miRNA and mRNA expression in five human cell types induced to senescence
Sprache	Englisch
Erscheinungsdatum	2024-04-10
Erscheinungsland	United States
Dokumenttyp	Preprint
DOI	10.1101/2024.04.10.588794
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Author Correction: Partial inhibition of mitochondrial complex I ameliorates Alzheimer's disease pathology and cognition in APP/PS1 female mice.

Stojakovic, Andrea / Trushin, Sergey / Sheu, Anthony / Khalili, Layla / Chang, Su-Youne / Li, Xing / Christensen, Trace / Salisbury, Jeffrey L / Geroux, Rachel E / Gateno, Benjamin / Flannery, Padraig J / Dehankar, Mrunal / Funk, Cory C / Wilkins, Jordan / Stepanova, Anna / O'Hagan, Tara / Galkin, Alexander / Nesbitt, Jarred / Zhu, Xiujuan /

Tripathi, Utkarsh / Macura, Slobodan / Tchkonia, Tamar / Pirtskhalava, Tamar / Kirkland, James L / Kudgus, Rachel A / Schoon, Renee A / Reid, Joel M / Yamazaki, Yu / Kanekiyo, Takahisa / Zhang, Song / Nemutlu, Emirhan / Dzeja, Petras / Jaspersen, Adam / Kwon, Ye In Christopher / Lee, Michael K / Trushina, Eugenia

Communications biology

2024 Band 7, Heft 1, Seite(n) 234

Sprache	Englisch
Erscheinungsdatum	2024-02-26
Erscheinungsland	England
Dokumenttyp	Published Erratum
ISSN	2399-3642
ISSN (online)	2399-3642
DOI	10.1038/s42003-024-05810-9
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Transplanting old organs promotes senescence in young recipients.

American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

2023 Band 24, Heft 3, Seite(n) 391–405

Abstract: In clinical organ transplantation, donor and recipient ages may differ substantially. Old donor organs accumulate senescent cells that have the capacity to induce senescence in naïve cells. We hypothesized that the engraftment of old organs may induce ... ...

Abstract	In clinical organ transplantation, donor and recipient ages may differ substantially. Old donor organs accumulate senescent cells that have the capacity to induce senescence in naïve cells. We hypothesized that the engraftment of old organs may induce senescence in younger recipients, promoting age-related pathologies. When performing isogeneic cardiac transplants between age-mismatched C57BL/6 old donor (18 months) mice and young and middle-aged C57BL/6 (3- or 12- month-old) recipients , we observed augmented frequencies of senescent cells in draining lymph nodes, adipose tissue, livers, and hindlimb muscles 30 days after transplantation. These observations went along with compromised physical performance and impaired spatial learning and memory abilities. Systemic levels of the senescence-associated secretory phenotype factors, including mitochondrial DNA (mt-DNA), were elevated in recipients. Of mechanistic relevance, injections of mt-DNA phenocopied effects of age-mismatched organ transplantation on accelerating aging. Single treatment of old donor animals with senolytics prior to transplantation attenuated mt-DNA release and improved physical capacities in young recipients. Collectively, we show that transplanting older organs induces senescence in transplant recipients, resulting in compromised physical and cognitive capacities. Depleting senescent cells with senolytics, in turn, represents a promising approach to improve outcomes of older organs.
Mesh-Begriff(e)	Animals ; Mice ; Cellular Senescence ; Senotherapeutics ; Mice, Inbred C57BL ; Organ Transplantation/adverse effects ; DNA/pharmacology ; Aging/physiology
Chemische Substanzen	Senotherapeutics ; DNA (9007-49-2)
Sprache	Englisch
Erscheinungsdatum	2023-10-31
Erscheinungsland	United States
Dokumenttyp	Journal Article
ZDB-ID	2060594-8
ISSN	1600-6143 ; 1600-6135
ISSN (online)	1600-6143
ISSN	1600-6135
DOI	10.1016/j.ajt.2023.10.013
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Orally-active, clinically-translatable senolytics restore α-Klotho in mice and humans.

EBioMedicine

2022 Band 77, Seite(n) 103912

Abstract: Background: α-Klotho is a geroprotective protein that can attenuate or alleviate deleterious changes with ageing and disease. Declines in α-Klotho play a role in the pathophysiology of multiple diseases and age-related phenotypes. Pre-clinical evidence ... ...

Abstract	Background: α-Klotho is a geroprotective protein that can attenuate or alleviate deleterious changes with ageing and disease. Declines in α-Klotho play a role in the pathophysiology of multiple diseases and age-related phenotypes. Pre-clinical evidence suggests that boosting α-Klotho holds therapeutic potential. However, readily clinically-translatable, practical strategies for increasing α-Klotho are not at hand. Here, we report that orally-active, clinically-translatable senolytics can increase α-Klotho in mice and humans. Methods: We examined α-Klotho expression in three different human primary cell types co-cultured with conditioned medium (CM) from senescent or non-senescent cells with or without neutralizing antibodies. We assessed α-Klotho expression in aged, obese, and senescent cell-transplanted mice treated with vehicle or senolytics. We assayed urinary α-Klotho in patients with idiopathic pulmonary fibrosis (IPF) who were treated with the senolytic drug combination, Dasatinib plus Quercetin (D+Q). Findings: We found exposure to the senescent cell secretome reduces α-Klotho in multiple nonsenescent human cell types. This was partially prevented by neutralizing antibodies against the senescence-associated secretory phenotype (SASP) factors, activin A and Interleukin 1α (IL-1α). Consistent with senescent cells' being a cause of decreased α-Klotho, transplanting senescent cells into younger mice reduced brain and urine α-Klotho. Selectively removing senescent cells genetically or pharmacologically increased α-Klotho in urine, kidney, and brain of mice with increased senescent cell burden, including naturally-aged, diet-induced obese (DIO), or senescent cell-transplanted mice. D+Q increased α-Klotho in urine of patients with IPF, a disease linked to cellular senescence. Interpretation: Senescent cells cause reduced α-Klotho, partially due to their production of activin A and IL-1α. Targeting senescent cells boosts α-Klotho in mice and humans. Thus, clearing senescent cells restores α-Klotho, potentially opening a novel, translationally-feasible avenue for developing orally-active small molecule, α-Klotho-enhancing clinical interventions. Furthermore, urinary α-Klotho may prove to be a useful test for following treatments in senolytic clinical trials. Funding: This work was supported by National Institute of Health grants AG013925 (J.L.K.), AG062413 (J.L.K., S.K.), AG044271 (N.M.), AG013319 (N.M.), and the Translational Geroscience Network (AG061456: J.L.K., T.T., N.M., S.B.K., S.K.), Robert and Arlene Kogod (J.L.K.), the Connor Group (J.L.K.), Robert J. and Theresa W. Ryan (J.L.K.), and the Noaber Foundation (J.L.K.). The previous IPF clinical trial was supported by the Claude D. Pepper Older Americans Independence Centers at WFSM (AG021332: J.N.J., S.B.K.), UTHSCA (AG044271: A.M.N.), and the Translational Geroscience Network.
Mesh-Begriff(e)	Aged ; Aging ; Animals ; Brain ; Cellular Senescence ; Humans ; Mice ; Quercetin/pharmacology ; Senotherapeutics
Chemische Substanzen	Senotherapeutics ; Quercetin (9IKM0I5T1E)
Sprache	Englisch
Erscheinungsdatum	2022-03-13
Erscheinungsland	Netherlands
Dokumenttyp	Journal Article
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2022.103912
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: SARS-CoV-2 causes senescence in human cells and exacerbates the senescence-associated secretory phenotype through TLR-3.

Tripathi, Utkarsh / Nchioua, Rayhane / Prata, Larissa G P Langhi / Zhu, Yi / Gerdes, Erin O Wissler / Giorgadze, Nino / Pirtskhalava, Tamar / Parker, Erik / Xue, Ailing / Espindola-Netto, Jair Machado / Stenger, Steffen / Robbins, Paul D / Niedernhofer, Laura J / Dickinson, Stephanie L / Allison, David B / Kirchhoff, Frank / Sparrer, Konstantin Maria Johannes / Tchkonia, Tamar / Kirkland, James L

Aging

2021 Band 13, Heft 18, Seite(n) 21838–21854

Abstract: Senescent cells, which arise due to damage-associated signals, are apoptosis-resistant and can express a pro-inflammatory, tissue-destructive senescence-associated secretory phenotype (SASP). We recently reported that a component of the severe acute ... ...

Abstract	Senescent cells, which arise due to damage-associated signals, are apoptosis-resistant and can express a pro-inflammatory, tissue-destructive senescence-associated secretory phenotype (SASP). We recently reported that a component of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) surface protein, S1, can amplify the SASP of senescent cultured human cells and that a related mouse β-coronavirus, mouse hepatitis virus (MHV), increases SASP factors and senescent cell burden in infected mice. Here, we show that SARS-CoV-2 induces senescence in human non-senescent cells and exacerbates the SASP in human senescent cells through Toll-like receptor-3 (TLR-3). TLR-3, which senses viral RNA, was increased in human senescent compared to non-senescent cells. Notably, genetically or pharmacologically inhibiting TLR-3 prevented senescence induction and SASP amplification by SARS-CoV-2 or Spike pseudotyped virus. While an artificial TLR-3 agonist alone was not sufficient to induce senescence, it amplified the SASP in senescent human cells. Consistent with these findings, lung p16
Mesh-Begriff(e)	Aging ; Animals ; Apoptosis ; COVID-19/metabolism ; COVID-19/virology ; Cellular Senescence ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Humans ; Inflammation ; Lung/metabolism ; Mice ; Phenotype ; SARS-CoV-2/pathogenicity ; Toll-Like Receptor 3/metabolism ; Viral Proteins ; COVID-19 Drug Treatment
Chemische Substanzen	CDKN2A protein, human ; Cyclin-Dependent Kinase Inhibitor p16 ; TLR3 protein, human ; Toll-Like Receptor 3 ; Viral Proteins
Sprache	Englisch
Erscheinungsdatum	2021-09-16
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.203560
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Whole-body senescent cell clearance alleviates age-related brain inflammation and cognitive impairment in mice.

Aging cell

2021 Band 20, Heft 2, Seite(n) e13296

Abstract: Cellular senescence is characterized by an irreversible cell cycle arrest and a pro-inflammatory senescence-associated secretory phenotype (SASP), which is a major contributor to aging and age-related diseases. Clearance of senescent cells has been shown ...

Abstract	Cellular senescence is characterized by an irreversible cell cycle arrest and a pro-inflammatory senescence-associated secretory phenotype (SASP), which is a major contributor to aging and age-related diseases. Clearance of senescent cells has been shown to improve brain function in mouse models of neurodegenerative diseases. However, it is still unknown whether senescent cell clearance alleviates cognitive dysfunction during the aging process. To investigate this, we first conducted single-nuclei and single-cell RNA-seq in the hippocampus from young and aged mice. We observed an age-dependent increase in p16
Mesh-Begriff(e)	Age Factors ; Animals ; Cellular Senescence ; Cognitive Dysfunction/metabolism ; Cognitive Dysfunction/pathology ; Cyclin-Dependent Kinase Inhibitor p16/metabolism ; Encephalitis/metabolism ; Encephalitis/pathology ; Mice ; Mice, Transgenic
Chemische Substanzen	Cyclin-Dependent Kinase Inhibitor p16
Sprache	Englisch
Erscheinungsdatum	2021-01-20
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.13296
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Deleted in breast cancer 1 limits adipose tissue fat accumulation and plays a key role in the development of metabolic syndrome phenotype.

Escande, Carlos / Nin, Veronica / Pirtskhalava, Tamar / Chini, Claudia C S / Tchkonia, Tamar / Kirkland, James L / Chini, Eduardo N

Diabetes

2014 Band 64, Heft 1, Seite(n) 12–22

Abstract: Obesity is often regarded as the primary cause of metabolic syndrome. However, many lines of evidence suggest that obesity may develop as a protective mechanism against tissue damage during caloric surplus and that it is only when the maximum fat ... ...

Abstract	Obesity is often regarded as the primary cause of metabolic syndrome. However, many lines of evidence suggest that obesity may develop as a protective mechanism against tissue damage during caloric surplus and that it is only when the maximum fat accumulation capacity is reached and fatty acid spillover occurs into to peripheral tissues that metabolic diseases develop. In this regard, identifying the molecular mechanisms that modulate adipocyte fat accumulation and fatty acid spillover is imperative. Here we identify the deleted in breast cancer 1 (DBC1) protein as a key regulator of fat storage capacity of adipocytes. We found that knockout (KO) of DBC1 facilitated fat cell differentiation and lipid accumulation and increased fat storage capacity of adipocytes in vitro and in vivo. This effect resulted in a "healthy obesity" phenotype. DBC1 KO mice fed a high-fat diet, although obese, remained insulin sensitive, had lower free fatty acid in plasma, were protected against atherosclerosis and liver steatosis, and lived longer. We propose that DBC1 is part of the molecular machinery that regulates fat storage capacity in adipocytes and participates in the "turn-off" switch that limits adipocyte fat accumulation and leads to fat spillover into peripheral tissues, leading to the deleterious effects of caloric surplus.
Mesh-Begriff(e)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/metabolism ; Adipocytes/cytology ; Adipocytes/metabolism ; Animals ; Aorta/cytology ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Cell Differentiation/physiology ; Cells, Cultured ; Endothelial Cells/cytology ; Endothelial Cells/metabolism ; Fatty Acids, Nonesterified/blood ; Fatty Liver/genetics ; Fatty Liver/metabolism ; Female ; Glycerol/metabolism ; Humans ; Metabolic Syndrome/genetics ; Metabolic Syndrome/metabolism ; Mice, Knockout ; Obesity/genetics ; Obesity/metabolism ; Phenotype ; Sirtuin 1/metabolism ; Stem Cells/cytology ; Stromal Cells/cytology
Chemische Substanzen	Adaptor Proteins, Signal Transducing ; CCAR2 protein, human ; Fatty Acids, Nonesterified ; KIAA1967 protein, mouse ; SIRT1 protein, human (EC 3.5.1.-) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; Glycerol (PDC6A3C0OX)
Sprache	Englisch
Erscheinungsdatum	2014-07-22
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db14-0192
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: New agents that target senescent cells: the flavone, fisetin, and the BCL-X

Zhu, Yi / Doornebal, Ewald J / Pirtskhalava, Tamar / Giorgadze, Nino / Wentworth, Mark / Fuhrmann-Stroissnigg, Heike / Niedernhofer, Laura J / Robbins, Paul D / Tchkonia, Tamara / Kirkland, James L

Aging

2017 Band 9, Heft 3, Seite(n) 955–963

Abstract: Senescent cells accumulate with aging and at sites of pathology in multiple chronic diseases. Senolytics are drugs that selectively promote apoptosis of senescent cells by temporarily disabling the pro-survival pathways that enable senescent cells to ... ...

Abstract	Senescent cells accumulate with aging and at sites of pathology in multiple chronic diseases. Senolytics are drugs that selectively promote apoptosis of senescent cells by temporarily disabling the pro-survival pathways that enable senescent cells to resist the pro-apoptotic, pro-inflammatory factors that they themselves secrete. Reducing senescent cell burden by genetic approaches or by administering senolytics delays or alleviates multiple age- and disease-related adverse phenotypes in preclinical models. Reported senolytics include dasatinib, quercetin, navitoclax (ABT263), and piperlongumine. Here we report that fisetin, a naturally-occurring flavone with low toxicity, and A1331852 and A1155463, selective BCL-X
Mesh-Begriff(e)	Aniline Compounds/pharmacology ; Antineoplastic Agents/pharmacology ; Apoptosis/drug effects ; Cell Line ; Cell Survival/drug effects ; Cellular Senescence/drug effects ; Flavonoids/pharmacology ; Humans ; Sulfonamides/pharmacology ; bcl-X Protein/antagonists & inhibitors
Chemische Substanzen	Aniline Compounds ; Antineoplastic Agents ; BCL2L1 protein, human ; Flavonoids ; Sulfonamides ; bcl-X Protein ; fisetin (OO2ABO9578) ; navitoclax (XKJ5VVK2WD)
Sprache	Englisch
Erscheinungsdatum	2017-03-07
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1945-4589
ISSN (online)	1945-4589
DOI	10.18632/aging.101202
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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