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Article ; Online: A conversation with Judith Campisi: Leader in the field of aging research.

Schafer, Marissa J / Campisi, Judith / Niedernhofer, Laura J

2021 Volume 69, Page(s) 101366

MeSH term(s)	Aging ; Humans
Language	English
Publishing date	2021-05-17
Publishing country	England
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2075672-0
ISSN	1872-9649 ; 1568-1637
ISSN (online)	1872-9649
ISSN	1568-1637
DOI	10.1016/j.arr.2021.101366
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Article: The Role of Senescent Cells in Acquired Drug Resistance and Secondary Cancer in BRAFi-Treated Melanoma.

Thompson, Elizabeth L / Hu, Jiayi J / Niedernhofer, Laura J

Cancers

2021 Volume 13, Issue 9

Abstract: ... ...

Abstract	BRAF
Language	English
Publishing date	2021-05-07
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13092241
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Article ; Online: Epigenetics, DNA damage, and aging.

Soto-Palma, Carolina / Niedernhofer, Laura J / Faulk, Christopher D / Dong, Xiao

The Journal of clinical investigation

2022 Volume 132, Issue 16

Abstract: Over the course of a human lifespan, genome integrity erodes, leading to an increased abundance of several types of chromatin changes. The abundance of DNA lesions (chemical perturbations to nucleotides) increases with age, as does the number of genomic ... ...

Abstract	Over the course of a human lifespan, genome integrity erodes, leading to an increased abundance of several types of chromatin changes. The abundance of DNA lesions (chemical perturbations to nucleotides) increases with age, as does the number of genomic mutations and transcriptional disruptions caused by replication or transcription of those lesions, respectively. At the epigenetic level, precise DNA methylation patterns degrade, likely causing increasingly stochastic variations in gene expression. Similarly, the tight regulation of histone modifications begins to unravel. The genomic instability caused by these mechanisms allows transposon element reactivation and remobilization, further mutations, gene dysregulation, and cytoplasmic chromatin fragments. This cumulative genomic instability promotes cell signaling events that drive cell fate decisions and extracellular communications known to disrupt tissue homeostasis and regeneration. In this Review, we focus on age-related epigenetic changes and their interactions with age-related genomic changes that instigate these events.
MeSH term(s)	Aging/genetics ; Aging/metabolism ; Chromatin/chemistry ; Chromatin/genetics ; Chromatin/metabolism ; DNA Damage ; DNA Methylation/physiology ; Epigenesis, Genetic ; Genomic Instability ; Histones/metabolism ; Humans ; Mutation ; Signal Transduction/genetics ; Signal Transduction/physiology ; Stochastic Processes
Chemical Substances	Chromatin ; Histones
Language	English
Publishing date	2022-08-23
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI158446
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Article ; Online: Senotherapeutics for healthy ageing.

Niedernhofer, Laura J / Robbins, Paul D

Nature reviews. Drug discovery

2018 Volume 17, Issue 5, Page(s) 377

MeSH term(s)	Aging ; Cellular Senescence ; Healthy Aging
Language	English
Publishing date	2018-04-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	2062954-0
ISSN	1474-1784 ; 1474-1776
ISSN (online)	1474-1784
ISSN	1474-1776
DOI	10.1038/nrd.2018.44
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Zs.A 5564: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article ; Online: The Role of DNA Repair in Immunological Diversity: From Molecular Mechanisms to Clinical Ramifications.

Gullickson, Peter / Xu, Yunwen W / Niedernhofer, Laura J / Thompson, Elizabeth L / Yousefzadeh, Matthew J

Frontiers in immunology

2022 Volume 13, Page(s) 834889

Abstract: ... for the successful completion of multiple immunological diversity processes: V(D)J recombination, class-switch ...

Abstract	An effective humoral immune response necessitates the generation of diverse and high-affinity antibodies to neutralize pathogens and their products. To generate this assorted immune repertoire, DNA damage is introduced at specific regions of the genome. Purposeful genotoxic insults are needed for the successful completion of multiple immunological diversity processes: V(D)J recombination, class-switch recombination, and somatic hypermutation. These three processes, in concert, yield a broad but highly specific immune response. This review highlights the importance of DNA repair mechanisms involved in each of these processes and the catastrophic diseases that arise from DNA repair deficiencies impacting immune system function. These DNA repair disorders underline not only the importance of maintaining genomic integrity for preventing disease but also for robust adaptive immunity.
MeSH term(s)	DNA Damage ; DNA Repair ; Immunity, Humoral/genetics ; Immunoglobulin Class Switching ; V(D)J Recombination
Language	English
Publishing date	2022-04-01
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.834889
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Article ; Online: Cellular senescence: a key therapeutic target in aging and diseases.

Zhang, Lei / Pitcher, Louise E / Yousefzadeh, Matthew J / Niedernhofer, Laura J / Robbins, Paul D / Zhu, Yi

The Journal of clinical investigation

2022 Volume 132, Issue 15

Abstract: Cellular senescence is a hallmark of aging defined by stable exit from the cell cycle in response to cellular damage and stress. Senescent cells (SnCs) can develop a characteristic pathogenic senescence-associated secretory phenotype (SASP) that drives ... ...

Abstract	Cellular senescence is a hallmark of aging defined by stable exit from the cell cycle in response to cellular damage and stress. Senescent cells (SnCs) can develop a characteristic pathogenic senescence-associated secretory phenotype (SASP) that drives secondary senescence and disrupts tissue homeostasis, resulting in loss of tissue repair and regeneration. The use of transgenic mouse models in which SnCs can be genetically ablated has established a key role for SnCs in driving aging and age-related disease. Importantly, senotherapeutics have been developed to pharmacologically eliminate SnCs, termed senolytics, or suppress the SASP and other markers of senescence, termed senomorphics. Based on extensive preclinical studies as well as small clinical trials demonstrating the benefits of senotherapeutics, multiple clinical trials are under way. This Review discusses the role of SnCs in aging and age-related diseases, strategies to target SnCs, approaches to discover and develop senotherapeutics, and preclinical and clinical advances of senolytics.
MeSH term(s)	Aging/genetics ; Aging/pathology ; Animals ; Cell Cycle ; Cellular Senescence/physiology ; Mice ; Mice, Transgenic ; Wound Healing
Language	English
Publishing date	2022-07-26
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	3067-3
ISSN	1558-8238 ; 0021-9738
ISSN (online)	1558-8238
ISSN	0021-9738
DOI	10.1172/JCI158450
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Article ; Online: Role of Cellular Senescence in Type II Diabetes.

Narasimhan, Akilavalli / Flores, Rafael R / Robbins, Paul D / Niedernhofer, Laura J

Endocrinology

2021 Volume 162, Issue 10

Abstract: Cellular senescence is a cell fate that occurs in response to numerous types of stress and can promote tissue repair or drive inflammation and disruption of tissue homeostasis depending on the context. Aging and obesity lead to an increase in the ... ...

Abstract	Cellular senescence is a cell fate that occurs in response to numerous types of stress and can promote tissue repair or drive inflammation and disruption of tissue homeostasis depending on the context. Aging and obesity lead to an increase in the senescent cell burden in multiple organs. Senescent cells release a myriad of senescence-associated secretory phenotype factors that directly mediate pancreatic β-cell dysfunction, adipose tissue dysfunction, and insulin resistance in peripheral tissues, which promote the onset of type II diabetes mellitus. In addition, hyperglycemia and metabolic changes seen in diabetes promote cellular senescence. Diabetes-induced cellular senescence contributes to various diabetic complications. Thus, type II diabetes is both a cause and consequence of cellular senescence. This review summarizes recent studies on the link between aging, obesity, and diabetes, focusing on the role of cellular senescence in disease processes.
MeSH term(s)	Adipose Tissue/metabolism ; Adipose Tissue/pathology ; Aging/metabolism ; Animals ; Cardiovascular Diseases/metabolism ; Cellular Senescence ; Diabetes Mellitus, Type 2/metabolism ; Diabetes Mellitus, Type 2/physiopathology ; Diabetic Nephropathies/pathology ; Diabetic Retinopathy/metabolism ; Disease Models, Animal ; Humans ; Hyperglycemia/metabolism ; Immune System ; Inflammation ; Insulin/metabolism ; Insulin Resistance ; Insulin-Secreting Cells/metabolism ; Mice ; Obesity/metabolism ; Phenotype ; Senescence-Associated Secretory Phenotype ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Insulin ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-08-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/endocr/bqab136
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Article ; Online: Targeting Cellular Senescence with Senotherapeutics: Development of New Approaches for Skin Care.

Thompson, Elizabeth L / Pitcher, Louise E / Niedernhofer, Laura J / Robbins, Paul D

Plastic and reconstructive surgery

2021 Volume 150, Page(s) 12S–19S

Abstract: Summary: Aging of the skin is evidenced by increased wrinkles, age spots, dryness, and thinning with decreased elasticity. Extrinsic and intrinsic factors including UV, pollution, and inflammation lead to an increase in senescent cells (SnCs) in skin ... ...

Abstract	Summary: Aging of the skin is evidenced by increased wrinkles, age spots, dryness, and thinning with decreased elasticity. Extrinsic and intrinsic factors including UV, pollution, and inflammation lead to an increase in senescent cells (SnCs) in skin with age that contribute to these observed pathological changes. Cellular senescence is induced by multiple types of damage and stress and is characterized by the irreversible exit from the cell cycle with upregulation of cell cycle-dependent kinase inhibitors p16INK4a and p21CIP1. Most SnCs also developed an inflammatory senescence-associated secretory phenotype (SASP) that drives further pathology through paracrine effects on neighboring cells and endocrine effects on cells at a distance. Recently, compounds able to kill senescent cells specifically, termed senolytics, or suppress the SASP, termed senomorphics, have been developed that have the potential to improve skin aging as well as systemic aging in general. Here, we provide a summary of the evidence for a key role in cellular senescence in driving skin aging. In addition, the evidence for the potential application of senotherapeutics for skin treatments is presented. Overall, topical, and possibly oral senotherapeutic treatments have tremendous potential to eventually become a standard of care for skin aging and related skin disorders.
MeSH term(s)	Cellular Senescence ; Humans ; Inflammation ; Senotherapeutics ; Skin Care
Chemical Substances	Senotherapeutics
Language	English
Publishing date	2021-09-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	208012-6
ISSN	1529-4242 ; 0032-1052 ; 0096-8501
ISSN (online)	1529-4242
ISSN	0032-1052 ; 0096-8501
DOI	10.1097/PRS.0000000000009668
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Article ; Online: Targeting cellular senescence with senotherapeutics: senolytics and senomorphics.

Zhang, Lei / Pitcher, Louise E / Prahalad, Vaishali / Niedernhofer, Laura J / Robbins, Paul D

The FEBS journal

2022 Volume 290, Issue 5, Page(s) 1362–1383

Abstract: The concept of geroscience is that since ageing is the greatest risk factor for many diseases and conditions, targeting the ageing process itself will have the greatest impact on human health. Of the hallmarks of ageing, cellular senescence has emerged ... ...

Abstract	The concept of geroscience is that since ageing is the greatest risk factor for many diseases and conditions, targeting the ageing process itself will have the greatest impact on human health. Of the hallmarks of ageing, cellular senescence has emerged as a druggable therapeutic target for extending healthspan in model organisms. Cellular senescence is a cell state of irreversible proliferative arrest driven by different types of stress, including oncogene-induced stress. Many senescent cells (SnCs) develop a senescent-associated secretory phenotype (SASP) comprising pro-inflammatory cytokines, chemokines, proteases, bioactive lipids, inhibitory molecules, extracellular vesicles, metabolites, lipids and other factors, able to promote chronic inflammation and tissue dysfunction. SnCs up-regulate senescent cell anti-apoptotic pathways (SCAPs) that prevent them from dying despite the accumulation of damage to DNA and other organelles. These SCAPs and other pathways altered in SnCs represent therapeutic targets for the development of senotherapeutic drugs that induce selective cell death of SnCs, specifically termed senolytics or suppress markers of senescence, in particular the SASP, termed senomorphics. Here, we review the current state of the development of senolytics and senomorphics for the treatment of age-related diseases and disorders and extension of healthy longevity. In addition, the challenges of documenting senolytic and senomorphic activity in pre-clinical models and the current state of the clinical application of the different senotherapeutics will be discussed.
MeSH term(s)	Humans ; Senotherapeutics ; Cellular Senescence ; Aging/physiology ; Longevity ; Lipids
Chemical Substances	Senotherapeutics ; Lipids
Language	English
Publishing date	2022-02-01
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2173655-8
ISSN	1742-4658 ; 1742-464X
ISSN (online)	1742-4658
ISSN	1742-464X
DOI	10.1111/febs.16350
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Article ; Online: COVID-19 and cellular senescence.

Schmitt, Clemens A / Tchkonia, Tamar / Niedernhofer, Laura J / Robbins, Paul D / Kirkland, James L / Lee, Soyoung

Nature reviews. Immunology

2022 Volume 23, Issue 4, Page(s) 251–263

Abstract: The clinical severity of coronavirus disease 2019 (COVID-19) is largely determined by host factors. Recent advances point to cellular senescence, an ageing-related switch in cellular state, as a critical regulator of SARS-CoV-2-evoked hyperinflammation. ... ...

Abstract	The clinical severity of coronavirus disease 2019 (COVID-19) is largely determined by host factors. Recent advances point to cellular senescence, an ageing-related switch in cellular state, as a critical regulator of SARS-CoV-2-evoked hyperinflammation. SARS-CoV-2, like other viruses, can induce senescence and exacerbates the senescence-associated secretory phenotype (SASP), which is comprised largely of pro-inflammatory, extracellular matrix-degrading, complement-activating and pro-coagulatory factors secreted by senescent cells. These effects are enhanced in elderly individuals who have an increased proportion of pre-existing senescent cells in their tissues. SASP factors can contribute to a 'cytokine storm', tissue-destructive immune cell infiltration, endothelialitis (endotheliitis), fibrosis and microthrombosis. SASP-driven spreading of cellular senescence uncouples tissue injury from direct SARS-CoV-2-inflicted cellular damage in a paracrine fashion and can further amplify the SASP by increasing the burden of senescent cells. Preclinical and early clinical studies indicate that targeted elimination of senescent cells may offer a novel therapeutic opportunity to attenuate clinical deterioration in COVID-19 and improve resilience following infection with SARS-CoV-2 or other pathogens.
MeSH term(s)	Humans ; COVID-19 ; SARS-CoV-2 ; Cellular Senescence/physiology ; Aging
Language	English
Publishing date	2022-10-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2062776-2
ISSN	1474-1741 ; 1474-1733
ISSN (online)	1474-1741
ISSN	1474-1733
DOI	10.1038/s41577-022-00785-2
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