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Senescence of Activated Stellate Cells Limits Liver Fibrosis
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In the citing paper
“There are a number of theoretical side effects of eliminating senescent cells, including impaired wound healing or fibrosis during liver regeneration (Krizhanovsky et al., 2008; Demaria et al., 2014).”
From The Achilles' heel of senescent cells: from transcriptome to senolytic drugs (2015) · cites this paper as Krizhanovsky et al., 2008
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In the citing paper
“Preclinical studies have shown that SnC clearance can impair liver regeneration and wound healing under certain conditions, emphasizing the need to differentiate transient, beneficial senescence from chronic, pathological accumulation133–135.”
From Emerging strategies in senotherapeutics: from broad-spectrum senolysis to precision reprogramming (2026) · cites this paper as [134]
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Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Among the cells that participate in the clearance of senescent cells are natural killer cells, macrophages, and T cells (131, 135, 139).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [139]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In a mouse model of acute liver injury, the injury induced the senescence of hepatic stellate cells, which were eventually cleared by the immune system (principally by natural killer cells) (139).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [139]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“When the injury was performed on mice that were deficient in the p53/p21 and p16INK4a/pRB pathways—that is, mice deficient in undergoing a senescence response—healing was accompanied by a marked increase in fibrosis (139).”
From Aging, Cellular Senescence, and Cancer (2013) · cites this paper as [139]
Experimental — accuracy not yet measured
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“SASP from these cells attracts natural killer (NK) cells that eliminate senescent cells from the liver to restore liver homeostasis145.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [145]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Cellular senescence contributes to the maintenance of the structure and the function of tissues following injury.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [145]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“The homeostatic function of senescent cells is dependent on their elimination by the immune system, once their beneficial functions have been performed145,151.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [145]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Senescence immunosurveillance is also essential to limit pathological fibrotic conditions and ageing20,145,151,157.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [145]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Among these cell types, NK cells, T cells and macrophages can physically interact with senescent cells in pathological and physiological conditions131,132,145,150,153–156.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [145]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Stimulation of innate immune response with poly(I:C), a simulator of viral infection, improves senescent cell clearance145.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [145]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Senescent cells are indeed subjected to immunosurveillance by multiple components of innate and adaptive immunity, including NK cells, T cells and macrophages145,151,153–156.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [145]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Mouse hepatic stellate cells have also been shown to exhibit senescence-associated markers such as SA-β-gal activity and expression of Cdkn1a, Cdkn2a and SASP components in models of liver injury163,164.”
From SenNet recommendations for detecting senescent cells in different tissues (2024) · cites this paper as [163]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Cellular senescence, a stress-induced irreversible growth arrest often characterized by p16 Ink4a expression and a distinctive secretory phenotype, prevents the proliferation of preneoplastic cells and has beneficial roles in tissue remodelling during embryogenesis and wound healing.”
From Naturally occurring p16Ink4a-positive cells shorten healthy lifespan (2016) · cites this paper as [7]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In response to liver injury, hepatic stellate cells (HSC) began to proliferate and produce extracellular matrixes for tissue repair before undergoing cellular senescence to prevent fibrosis.38, 39”
From Cellular senescence and senescence-associated secretory phenotype via the cGAS-STING signaling pathway in cancer (2020) · cites this paper as [39]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This pattern suggests a possible regulatory connection between PS fibroblasts and HSC activation, consistent with prior observations,49 though additional statistical power is needed for confirmation.”
From Cellular senescence in human liver under normal aging and cancer (2026) · cites this paper as [49]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“similar antifibrotic effects of senescent cells have been observed in the kidneys, liver and lungs in mouse models 10-12”
From Senescence and cancer — role and therapeutic opportunities (2022) · cites this paper as [10]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Senescent cells express surface-bound ligands and adhesion molecules that target them for attack by natural killer and other immune cells (Krizhanovsky et al., 2008)”
From Four faces of cellular senescence (2011) · cites this paper as Krizhanovsky et al., 2008
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Senescent stromal cells were shown to help resolve excessive fibrosis after skin or liver injury (Jun and Lau, 2010; Krizhanovsky et al., 2008).”
From An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA (2014) · cites this paper as Krizhanovsky et al., 2008
The cited source says what the claim attributes to it.
In the citing paper
“and the matrix metalloproteinases that comprise the SASP (Coppé et al., 2008, 2010b) were proposed to facilitate tissue repair by promoting collagen degradation, thereby limiting fibrosis (Jun and Lau, 2010; Krizhanovsky et al., 2008).”
From An Essential Role for Senescent Cells in Optimal Wound Healing through Secretion of PDGF-AA (2014) · cites this paper as Krizhanovsky et al., 2008
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“in liver fibrosis, a condition associated with scarring of the liver and decrease in its function, senescence limits the proliferation and expansion of ECM-producing activated hepatic stellate cells145,146. This response limits the progression of the pathology following liver damage.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [145]
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, recent studies showing that senescent cells have beneficial effects in injury repair and tissue remodelling 6 - 10 have called into question the simplistic view of senescence as only a driver of age-dependent pathologies, raising the specter that senescent cell clearance might remove useful cells in addition to detrimental ones.”
From Naturally occurring p16Ink4a-positive cells shorten healthy lifespan (2016) · cites this paper as [7]
The cited source says what the claim attributes to it.
In the citing paper
“By contrast, senescent cells have shown beneficial effects as tumour suppressors, during embryo development, and in liver and skin repair18–21 or reprogramming22–24.”
From Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration (2023) · cites this paper as [19]
The cited source says what the claim attributes to it.
In the citing paper
“Conversely, senescence is autonomously anti-proliferative, may be requisite for optimal cutaneous wound healing9 and may restrict pathological liver fibrosis10.”
From Cellular senescence mediates fibrotic pulmonary disease (2017) · cites this paper as [10]
The cited source says what the claim attributes to it.
In the citing paper
“The SASP can have a major impact on various biological processes, including cell proliferation, angiogenesis, inflammation16, epithelial-to-mesenchymal transition17, tissue repair18 and wound healing3 (Fig. 2).”
From Spatial mapping of cellular senescence: emerging challenges and opportunities (2023) · cites this paper as [18]
The cited source says what the claim attributes to it.
In the citing paper
“The SASP also contributes to the surveillance and elimination of senescent cells by the immune system 12-14 .”
From A complex secretory program orchestrated by the inflammasome controls paracrine senescence (2013) · cites this paper as [14]
The cited source says what the claim attributes to it.
In the citing paper
“Activation of hepatic stellate cells (HSCs) is the major source of ECM and the key driver of liver fibrosis [5].”
From Saikosaponin b1 Attenuates Liver Fibrosis by Blocking STAT3/Gli1 Interaction and Inducing Gli1 Degradation (2025) · cites this paper as [5]
The check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Specifically, the levels of PCNA and KI67 provide an estimation of which cell cycle phase a cell is in, with PCNA being at the highest level in the S phase and KI67 in the M phase9,10 (Fig. 1 B).”
From Guidelines for minimal information on cellular senescence experimentation in vivo (2024) · cites this paper as [9]
Experimental — accuracy not yet measuredThe check wasn’t confident either way, so it gives no verdict — never disputed.
In the citing paper
“Consistent with a beneficial role of senescent cells only for the duration of wound repair 6 - 8 , 18-month-old AP-treated ATTAC mice repaired cutaneous wounds when drug administration was suspended during healing (Extended Data Fig. 10ac).”
From Naturally occurring p16Ink4a-positive cells shorten healthy lifespan (2016) · cites this paper as [7]
Experimental — accuracy not yet measuredIn the citing paper
“The SASP also includes several chemokines and cytokines that activate immune cells to specifically target and eventually clear senescent cells from tissues”
From Redox control of senescence and age-related disease. (2017) · cites this paper as [85]
In the citing paper
“these secreted factors can stimulate the immune system to both suppress tumorigenesis and promote optimal repair of damaged tissues when senescent cells are removed after their beneficial actions (15–17).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [15]
In the citing paper
“This pathway can positively contribute to normal development and wound healing (15, 17, 61, 62).”
From The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. (2015) · cites this paper as [15]
In the citing paper
“However, these studies focused on the function of senescence in acute organ injury, not in chronic processes such as atherosclerosis.”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [207]
In the citing paper
“Experimental evidence shows that cellular senescence has roles in limiting myocardial206 and liver207 fibrosis, promoting skin healing,82 as well as in embryonal development,208 which have to be considered.”
From Senescence-induced inflammation: an important player and key therapeutic target in atherosclerosis (2020) · cites this paper as [207]
In the citing paper
“Recent data indicates that senescent cells play a variety of beneficial roles during processes such as embryonic development, tumor suppression, wound healing and tissue repair (Krizhanovsky et al., 2008, Muñoz-Espín et al., 2013, Demaria et al., 2014, Ritschka et al., 2017).”
From Telomeres and cell senescence—size matters not (2017) · cites this paper as Krizhanovsky et al., 2008
In the citing paper
“Elimination of these senescent cells by NK cells is needed to restrain liver fibrosis and return the liver to a predamaged state following short‐term damage”
From p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling (2017) · cites this paper as Krizhanovsky et al, 2008
In the citing paper
“In liver fibrosis activated stellate cells become senescent and exhibit activation of DDR.”
From p21 maintains senescent cell viability under persistent DNA damage response by restraining JNK and caspase signaling (2017) · cites this paper as Krizhanovsky et al, 2008
In the citing paper
“In a mouse model of carbon tetrachloride-induced liver fibrosis, the accumulation of senescent cells also functions to limit fibrosis [125].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [125]
In the citing paper
“The SASP also attracts innate immune cells that in turn eliminate the senescent HSCs and facilitate the resolution of fibrosis 94,120”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [120]
In the citing paper
“activated HSCs become senescent, exhibiting a typical SASP, including the expression of extracellular matrix degrading enzymes and proinflammatory cytokines.”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [120]
In the citing paper
“This was the first study to show that hepatic stellate cell senescence controls fibrosis through the SASP.”
From Inside and out: the activities of senescence in cancer (2014) · cites this paper as [120]
In the citing paper
“and recent evidence indicates that NK cells can recognize and eliminate senescent cells in vivo [43, 44].”
From Senescence of T Lymphocytes: Implications for Enhancing Human Immunity (2016) · cites this paper as [43]
In the citing paper
“Indeed, unlike chronic senescence (i.e., accumulation of deleterious senescent cells with aging), the acute induction of cellular senescence represents a transient physiological response during embryonic development [27,28] and adult tissue homeostasis (e.g., to facilitate tissue repair after liver damage, in skin fibrosis, and wound healing) [29,30,31].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [29]
In the citing paper
“Recruitment and activation of T cells and natural killer cells at the location of senescent cells in the tumor microenvironment or altered polarization of macrophages promote the removal of senescent or damaged cells [29,358,359,360].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [29]
In the citing paper
“SASP has recently been shown to have a beneficial effect on wound healing by recruiting immune cells to clear dead cells, promote angiogenesis, limit fibrosis, and stimulate wound closure (100, 111, 112).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [112]
In the citing paper
“Mounting evidence demonstrates that immune surveillance of senescent cells is executed by different immune cells such as macrophages, natural killer (NK) cells and cytotoxic T cells in cancer [5,130] and chronic liver cirrhosis [20].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [20]
In the citing paper
“For example, senescence-activated hepatic stellate cells upregulate cell-surface MICA and ULBP2, ligands of activating receptor NKG2D on NK cells [20].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [20]
In the citing paper
“NK cells are involved in the elimination of senescent cells through interaction between the activating NKG2D receptor and its ligands expressed on senescent cells.”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [20]
In the citing paper
“the YT human NK cell line preferentially destroys senescent IMR-90 fibroblasts [20].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [20]
In the citing paper
“NK cell activation by polyinosinic-polycytidylic acid [152] decreases the senescent cell number in the liver in vivo, leading to reduced liver fibrosis [20].”
From Immune Clearance of Senescent Cells to Combat Ageing and Chronic Diseases (2020) · cites this paper as [20]
In the citing paper
“This may be in part attributable to the immunosurveillance of senescent cells by immune cells that can rapidly remove senescent cells to prevent the accumulation of senescent cells in vivo.34”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [34]
In the citing paper
“Furthermore, the SASP is involved in valuable physiological processes such as promoting tissue repair,18–20 fine-tuning the development of embryonic structures,21–23 and stimulating immune surveillance.24,25”
From Paracrine roles of cellular senescence in promoting tumourigenesis (2018) · cites this paper as [20]
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Citations
Cites
The serial cultivation of human diploid cell strains
Hayflick, L., & Moorhead, P. S. (1961) · Experimental Cell Research · doi:10.1016/0014-4827(61)90192-6 · Cited by 8,508
Oncogenic ras provokes premature cell senescence associated with accumulation of p53 and p16INK4a
Serrano, M., Lin, A. W., McCurrach, M. E., Beach, D., & Lowe, S. W. (1997) · Cell · doi:10.1016/s0092-8674(00)81902-9 · Cited by 5,218 · cited 7×
“To identify senescent cells in situ, we stained liver sections from CCl4 and vehicle-treated (control) mice for a panel of senescence-associated markers, including SA-b-gal and proteins such as p16, p21, p53, and Hmga1, which have been causally linked to the senescence program (Collado et al., 2007; Narita et al., 200…”
BackgroundMethodInfluentialSelf-citationBataller, R., & Brenner, D. A. (2005) · Journal of Clinical Investigation · doi:10.1172/jci24282 · Cited by 4,958
Cellular senescence: when bad things happen to good cells
Campisi, J., & d'Adda di Fagagna, F. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2233 · Cited by 4,441
Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas
Xue, W., Zender, L., Miething, C., Dickins, R. A., Hernando, E., Krizhanovsky, V., Cordon-Cardo, C., & Lowe, S. W. (2007) · Nature · doi:10.1038/nature05529 · Cited by 2,473
Self-citationRb-mediated heterochromatin formation and silencing of E2F target genes during cellular senescence
Narita, M., Nuñez, S., Heard, E., Narita, M., Lin, A. W., Hearn, S. A., Spector, D. L., Hannon, G. J., & Lowe, S. W. (2003) · Cell · doi:10.1016/s0092-8674(03)00401-x · Cited by 2,278 · cited 8×
“V12 as described ( Narita et al., 2003 ). For in vitro cytotoxicity assays, growing or senescent cells were plated in 6-well plates at 50,000 cells per well.”
BackgroundMethodInfluentialSelf-citationBRAFE600-associated senescence-like cell cycle arrest of human naevi
Michaloglou, C., Vredeveld, L. C. W., Soengas, M. S., Denoyelle, C., Kuilman, T., van der Horst, C. M. A. M., Majoor, D. M., Shay, J. W., Mooi, W. J., & Peeper, D. S. (2005) · Nature · doi:10.1038/nature03890 · Cited by 2,160
Crucial role of p53-dependent cellular senescence in suppression of Pten-deficient tumorigenesis
Chen, Z., Trotman, L. C., Shaffer, D., Lin, H.-K., Dotan, Z. A., Niki, M., Koutcher, J. A., Scher, H. I., Ludwig, T., Gerald, W., et al. (2005) · Nature · doi:10.1038/nature03918 · Cited by 1,993
Oncogene-induced senescence is part of the tumorigenesis barrier imposed by DNA damage checkpoints
Bartkova, J., Rezaei, N., Liontos, M., Karakaidos, P., Kletsas, D., Issaeva, N., Vassiliou, L.-V. F., Kolettas, E., Niforou, K., Zoumpourlis, V. C., et al. (2006) · Nature · doi:10.1038/nature05268 · Cited by 1,986
Oncogene-induced senescence is a DNA damage response triggered by DNA hyper-replication
Di Micco, R., Fumagalli, M., Cicalese, A., Piccinin, S., Gasparini, P., Luise, C., Schurra, C., Garre’, M., Giovanni Nuciforo, P., Bensimon, A., et al. (2006) · Nature · doi:10.1038/nature05327 · Cited by 1,821
Flagged first, then by citations
Cited by
Sorted by citations
Items 101–200 of 1,008
NK cell–mediated cytotoxicity contributes to tumor control by a cytostatic drug combination
Ruscetti, M., Leibold, J., Bott, M. J., Fennell, M., Kulick, A., Salgado, N. R., Chen, C.-C., Ho, Y.-J., Sanchez-Rivera, F. J., Feucht, J., et al. (2018) · Science · doi:10.1126/science.aas9090 · Cited by 415
Self-citationSenolysis by glutaminolysis inhibition ameliorates various age-associated disorders
Johmura, Y., Yamanaka, T., Omori, S., Wang, T.-W., Sugiura, Y., Matsumoto, M., Suzuki, N., Kumamoto, S., Yamaguchi, K., Hatakeyama, S., et al. (2021) · Science · doi:10.1126/science.abb5916 · Cited by 440
Senescence-Induced Vascular Remodeling Creates Therapeutic Vulnerabilities in Pancreas Cancer
Ruscetti, M., Morris, J. P., Mezzadra, R., Russell, J., Leibold, J., Romesser, P. B., Simon, J., Kulick, A., Ho, Y.-J., Fennell, M., et al. (2020) · Cell · doi:10.1016/j.cell.2020.03.008 · Cited by 424
Self-citationBRD4 Connects Enhancer Remodeling to Senescence Immune Surveillance
Tasdemir, N., Banito, A., Roe, J.-S., Alonso-Curbelo, D., Camiolo, M., Tschaharganeh, D. F., Huang, C.-H., Aksoy, O., Bolden, J. E., Chen, C.-C., et al. (2016) · Cancer Discovery · doi:10.1158/2159-8290.cd-16-0217 · Cited by 415
“These immune-modulatory activities may be important for the resolution of certain wound-healing responses (9, 10, 13) and underlie a unique form of immune surveillance that can eliminate premalignant or malignant cells undergoing senescence in vivo (33, 35, 36).”
InfluentialSelf-citationDNA Damage-Mediated Induction of a Chemoresistant Niche
Gilbert, L. A., & Hemann, M. T. (2010) · Cell · doi:10.1016/j.cell.2010.09.043 · Cited by 428
Mechanisms of liver fibrosis and its role in liver cancer
Dhar, D., Baglieri, J., Kisseleva, T., & Brenner, D. A. (2020) · Experimental Biology and Medicine · doi:10.1177/1535370219898141 · Cited by 449
How does SIRT1 affect metabolism, senescence and cancer?
Brooks, C. L., & Gu, W. J. (2008) · Nature reviews. Cancer · doi:10.1038/nrc2562 · Cited by 434
Cellular senescence: a link between cancer and age-related degenerative disease?
Campisi, J., Andersen, J. K., Kapahi, P., & Melov, S. (2011) · Seminars in Cancer Biology · doi:10.1016/j.semcancer.2011.09.001 · Cited by 421
Telomeres and cell senescence—size matters not
Victorelli, S., & Passos, J. F. (2017) · EBioMedicine · doi:10.1016/j.ebiom.2017.03.027 · Cited by 413
Senescence-associated inflammatory responses: aging and cancer perspectives
Lasry, A., & Ben-Neriah, Y. (2015) · Trends in Immunology · doi:10.1016/j.it.2015.02.009 · Cited by 408
Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration
Moiseeva, V., Cisneros, A., Sica, V., Deryagin, O., Lai, Y., Jung, S., Andrés, E., An, J., Segalés, J., Ortet, L., et al. (2023) · Nature · doi:10.1038/s41586-022-05535-x · Cited by 423
Quantitative identification of senescent cells in aging and disease
Biran, A., Zada, L., Abou Karam, P., Vadai, E., Roitman, L., Ovadya, Y., Porat, Z., & Krizhanovsky, V. (2017) · Aging Cell · doi:10.1111/acel.12592 · Cited by 402
Self-citationIannello, A., Thompson, T. W., Ardolino, M., Lowe, S. W., & Raulet, D. H. (2013) · Journal of Experimental Medicine · doi:10.1084/jem.20130783 · Cited by 414
Self-citationBiomarkers of cellular senescence and skin aging
Wang, A. S., & Dreesen, O. (2018) · Frontiers in Genetics · doi:10.3389/fgene.2018.00247 · Cited by 404
Metabolic reprogramming in liver fibrosis
Horn, P., & Tacke, F. (2024) · Cell Metabolism · doi:10.1016/j.cmet.2024.05.003 · Cited by 432
Lehmann, M., Korfei, M., Mutze, K., Klee, S., Skronska-Wasek, W., Alsafadi, H. N., Ota, C., Costa, R., Schiller, H. B., Lindner, M., et al. (2017) · European Respiratory Journal · doi:10.1183/13993003.02367-2016 · Cited by 403
StellaTUM: current consensus and discussion on pancreatic stellate cell research
Erkan, M., Adler, G., Apte, M. V., Bachem, M. G., Buchholz, M., Detlefsen, S., Esposito, I., Frieß, H., Gress, T. M., Habisch, H., et al. (2011) · Gut · doi:10.1136/gutjnl-2011-301220 · Cited by 411
In situ elasticity modulation with dynamic substrates to direct cell phenotype
Kloxin, A. M., Benton, J. A., & Anseth, K. S. (2009) · Biomaterials · doi:10.1016/j.biomaterials.2009.09.025 · Cited by 415
SenNet recommendations for detecting senescent cells in different tissues
Suryadevara, V., Hudgins, A. D., Rajesh, A., Pappalardo, A., Karpova, A., Dey, A. K., Hertzel, A., Agudelo, A., Rocha, A., Soygur, B., et al. (2024) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-024-00738-8 · Cited by 408
Mechanisms and Regulation of Cellular Senescence
Roger, L., Tomas, F., & Gire, V. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222313173 · Cited by 395
Oncogenic stress sensed by the immune system: role of natural killer cell receptors
Raulet, D. H., & Guerra, N. (2009) · Nature reviews. Immunology · doi:10.1038/nri2604 · Cited by 405
DNA damage-how and why we age?
Yousefzadeh, M., Henpita, C., Vyas, R., Soto-Palma, C., Robbins, P., & Niedernhofer, L. (2021) · eLife · doi:10.7554/elife.62852 · Cited by 399
Recurrent turnover of senescent cells during regeneration of a complex structure
Yun, M. H., Davaapil, H., & Brockes, J. P. (2015) · eLife · doi:10.7554/elife.05505 · Cited by 385
Recognition of Tumors by the Innate Immune System and Natural Killer Cells
Marcus, A., Gowen, B. G., Thompson, T. W., Iannello, A., Ardolino, M., Deng, W., Wang, L., Shifrin, N. T., & Raulet, D. H. (2014) · Advances in immunology · doi:10.1016/b978-0-12-800267-4.00003-1 · Cited by 410
Immune ageing at single-cell resolution
Mogilenko, D. A., Shchukina, I., & Artyomov, M. N. (2021) · Nature reviews. Immunology · doi:10.1038/s41577-021-00646-4 · Cited by 396
Adverse outcome pathways: opportunities, limitations and open questions
Leist, M., Ghallab, A., Graepel, R., Marchan, R., Hassan, R., Bennekou, S. H., Limonciel, A., Vinken, M., Schildknecht, S., Waldmann, T., et al. (2017) · Archives of Toxicology · doi:10.1007/s00204-017-2045-3 · Cited by 394
Cellular and molecular mechanisms in the pathogenesis of liver fibrosis: An update
Elpek, G. Ö. (2014) · World Journal of Gastroenterology · doi:10.3748/wjg.v20.i23.7260 · Cited by 399
Aydin, M. M., & Akçalı, K. C. (2018) · The Turkish Journal of Gastroenterology · doi:10.5152/tjg.2018.17330 · Cited by 397
Bao, H., Cao, J., Chen, M., Min, C., Chen, W., Chen, X., Chen, Y., Chen, Y., Chen, Y., Chen, Z., et al. (2023) · Science China Life Sciences · doi:10.1007/s11427-023-2305-0 · Cited by 402
Evolving Concepts in the Pathogenesis of NASH: Beyond Steatosis and Inflammation
Peverill, W., Powell, L. W., & Skoien, R. (2014) · International Journal of Molecular Sciences · doi:10.3390/ijms15058591 · Cited by 387
Liver natural killer and natural killer T cells: immunobiology and emerging roles in liver diseases
Gao, B., Radaeva, S., & Park, O. (2009) · Journal of Leukocyte Biology · doi:10.1189/jlb.0309135 · Cited by 383
Guidelines for minimal information on cellular senescence experimentation in vivo
Ogrodnik, M., Carlos Acosta, J., Adams, P. D., d’Adda di Fagagna, F., Baker, D. J., Bishop, C. L., Chandra, T., Collado, M., Gil, J., Gorgoulis, V., et al. (2024) · Cell · doi:10.1016/j.cell.2024.05.059 · Cited by 376
Self-citationSex differences in cancer mechanisms
Rubin, J. B., Lagas, J. S., Broestl, L., Sponagel, J., Rockwell, N., Rhee, G., Rosen, S. F., Chen, S., Klein, R. S., Imoukhuede, P. I., et al. (2020) · Biology of Sex Differences · doi:10.1186/s13293-020-00291-x · Cited by 391
Brady, C. A., & Attardi, L. D. (2010) · Journal of Cell Science · doi:10.1242/jcs.064501 · Cited by 400
Cellular senescence: putting the paradoxes in perspective
Campisi, J. (2011) · Current Opinion in Genetics & Development · doi:10.1016/j.gde.2010.10.005 · Cited by 368
Cellular senescence in osteoarthritis pathology
McCulloch, K., Litherland, G. J., & Rai, T. S. (2017) · Aging Cell · doi:10.1111/acel.12562 · Cited by 367
Redox control of senescence and age-related disease.
Chandrasekaran, A., Idelchik, M. D. P. S., & Melendez, J. A. (2017) · Redox Biology · doi:10.1016/j.redox.2016.11.005 · Cited by 360
Santaguida, S., Richardson, A., Iyer, D., M’Saad, O., Zasadil, L. M., Knouse, K. A., Wong, Y. L., Rhind, N., Desai, A. B., & Amon, A. (2017) · Developmental Cell · doi:10.1016/j.devcel.2017.05.022 · Cited by 367
Role of immune cells in the removal of deleterious senescent cells
Kale, A., Sharma, A., Stolzing, A., Desprez, P.-Y., & Campisi, J. (2020) · Immunity & Ageing · doi:10.1186/s12979-020-00187-9 · Cited by 351
Opposing roles of hepatic stellate cell subpopulations in hepatocarcinogenesis
Filliol, A., Saito, Y., Nair, A., Dapito, D. H., Yu, L.-X., Ravichandra, A., Bhattacharjee, S., Affo, S., Fujiwara, N., Su, H., et al. (2022) · Nature · doi:10.1038/s41586-022-05289-6 · Cited by 349
Senescent cells and osteoarthritis: a painful connection
Jeon, O. H., David, N. E., Campisi, J., & Elisseeff, J. H. (2018) · Journal of Clinical Investigation · doi:10.1172/jci95147 · Cited by 359
Cellular Senescence Is Immunogenic and Promotes Antitumor Immunity
Marín, I., Boix, O., García-Garijo, A., Sirois, I., Caballé, A., Zarzuela, E., Ruano, I., Attolini, C. S., Prats, N., Lopez-Dominguez, J. A., et al. (2022) · Cancer Discovery · doi:10.1158/2159-8290.cd-22-0523 · Cited by 365
Cellular senescence in renal ageing and disease
Sturmlechner, I., Durik, M., Sieben, C. J., Baker, D. J., & van Deursen, J. M. (2017) · Nature Reviews Nephrology · doi:10.1038/nrneph.2016.183 · Cited by 345
Jun, J.-I., & Lau, L. F. (2018) · Journal of Clinical Investigation · doi:10.1172/jci93563 · Cited by 358
p53, cancer and the immune response
Blagih, J., Buck, M. D., & Vousden, K. H. (2020) · Journal of Cell Science · doi:10.1242/jcs.237453 · Cited by 333
Myofibroblasts: Trust your heart and let fate decide
Davis, J., & Molkentin, J. D. (2013) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2013.10.019 · Cited by 347
CCN1/CYR61: the very model of a modern matricellular protein
Lau, L. F. (2011) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-011-0778-3 · Cited by 338
NKG2D ligands mediate immunosurveillance of senescent cells
Sagiv, A., Burton, D. G. A., Moshayev, Z., Vadai, E., Wensveen, F., Ben-Dor, S., Golani, O., Polic, B., & Krizhanovsky, V. (2016) · Aging · doi:10.18632/aging.100897 · Cited by 345
Self-citationA versatile drug delivery system targeting senescent cells
Muñoz‐Espín, D., Rovira, M., Galiana, I., Giménez, C., Lozano‐Torres, B., Paez‐Ribes, M., Llanos, S., Chaib, S., Muñoz‐Martín, M., Ucero, A. C., et al. (2018) · EMBO Molecular Medicine · doi:10.15252/emmm.201809355 · Cited by 339
Stress, cell senescence and organismal ageing
de Magalhães, J. P., & Passos, J. F. (2018) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2017.07.001 · Cited by 316
Clearance of senescent decidual cells by uterine natural killer cells in cycling human endometrium
Brighton, P. J., Maruyama, Y., Fishwick, K., Vrljicak, P., Tewary, S., Fujihara, R., Muter, J., Lucas, E. S., Yamada, T., Woods, L., et al. (2017) · eLife · doi:10.7554/elife.31274 · Cited by 323
Healing and Hurting: Molecular Mechanisms, Functions, and Pathologies of Cellular Senescence
Adams, P. D. (2009) · Molecular Cell · doi:10.1016/j.molcel.2009.09.021 · Cited by 326
Borghesan, M., Fafián-Labora, J., Eleftheriadou, O., Carpintero-Fernández, P., Paez-Ribes, M., Vizcay-Barrena, G., Swisa, A., Kolodkin-Gal, D., Ximénez-Embún, P., Lowe, R., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.05.095 · Cited by 315
“, 2017); and (3) ex vivo mouse hepatic stellate cells (mHSCs) derived from an adult mouse harboring a doxycycline (Dox)inducible construct to express shp53 (Krizhanovsky et al., 2008; Lujambio et al., 2013) (Figure S1L).”
Aging and adipose tissue: potential interventions for diabetes and regenerative medicine
Palmer, A. K., & Kirkland, J. L. (2016) · Experimental Gerontology · doi:10.1016/j.exger.2016.02.013 · Cited by 324
Watanabe, S., Kawamoto, S., Ohtani, N., & Hara, E. (2017) · Cancer Science · doi:10.1111/cas.13184 · Cited by 321
Senescence from G2 arrest, revisited
Gire, V., & Dulić, V. (2015) · Cell Cycle · doi:10.1080/15384101.2014.1000134 · Cited by 300
Cells exhibiting strong p16 INK4a promoter activation in vivo display features of senescence
Liu, J.-Y., Souroullas, G. P., Diekman, B. O., Krishnamurthy, J., Hall, B. M., Sorrentino, J. A., Parker, J. S., Sessions, G. A., Gudkov, A. V., & Sharpless, N. E. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1818313116 · Cited by 306
Hazeldine, J., & Lord, J. M. (2013) · Ageing Research Reviews · doi:10.1016/j.arr.2013.04.003 · Cited by 328
Immune Modulation of Stem Cells and Regeneration
Aurora, A. B., & Olson, E. N. (2014) · Cell stem cell · doi:10.1016/j.stem.2014.06.009 · Cited by 322
Neuroinflammation in Alzheimer’s Disease
Onyango, I. G., Jauregui, G. V., Čarná, M., Bennett, J. P., & Stokin, G. B. (2021) · Biomedicines · doi:10.3390/biomedicines9050524 · Cited by 330
Adipose tissue aging: mechanisms and therapeutic implications
Ou, M., Zhang, H., Tan, P., Zhou, S., & Li, Q. (2022) · Cell Death and Disease · doi:10.1038/s41419-022-04752-6 · Cited by 352
Senescence of T Lymphocytes: Implications for Enhancing Human Immunity
Akbar, A. N., Henson, S. M., & Lanna, A. (2016) · Trends in Immunology · doi:10.1016/j.it.2016.09.002 · Cited by 285
Recent advancement of molecular mechanisms of liver fibrosis
Seki, E., & Brenner, D. A. (2015) · Journal of Hepato-Biliary-Pancreatic Sciences · doi:10.1002/jhbp.245 · Cited by 302
Yosef, R., Pilpel, N., Papismadov, N., Gal, H., Ovadya, Y., Vadai, E., Miller, S., Porat, Z., Ben‐Dor, S., & Krizhanovsky, V. (2017) · The EMBO Journal · doi:10.15252/embj.201695553 · Cited by 293
Self-citationCellular senescence in development, regeneration and disease
Rhinn, M., Ritschka, B., & Keyes, W. M. (2019) · Development · doi:10.1242/dev.151837 · Cited by 279
Ohtani, N. (2022) · Inflammation and Regeneration · doi:10.1186/s41232-022-00197-8 · Cited by 329
Cellular Senescence in the Kidney
Docherty, M.-H., O’Sullivan, E. D., Bonventre, J. V., & Ferenbach, D. A. (2019) · Journal of the American Society of Nephrology · doi:10.1681/asn.2018121251 · Cited by 291
Targeting senescent cells in translational medicine
Paez‐Ribes, M., González‐Gualda, E., Doherty, G. J., & Muñoz‐Espín, D. (2019) · EMBO Molecular Medicine · doi:10.15252/emmm.201810234 · Cited by 293
p21 produces a bioactive secretome that places stressed cells under immunosurveillance
Sturmlechner, I., Zhang, C., Sine, C. C., van Deursen, E.-J., Jeganathan, K. B., Hamada, N., Grasic, J., Friedman, D., Stutchman, J. T., Can, I., et al. (2021) · Science · doi:10.1126/science.abb3420 · Cited by 295
“Once established, senescent cells can persist in tissues and organs for prolonged periods of time (19), although they can also be recognized and eliminated by lymphocytes through mechanisms that remain ill-defined (4, 16, 20).”
BackgroundEmerging roles of the p38 MAPK and PI3K/AKT/mTOR pathways in oncogene-induced senescence
Xu, Y., Li, N., Xiang, R., & Sun, P. (2014) · Trends in Biochemical Sciences · doi:10.1016/j.tibs.2014.04.004 · Cited by 282
Natural killer cells in liver disease
Tian, Z., Chen, Y., & Gao, B. (2012) · Hepatology · doi:10.1002/hep.26115 · Cited by 306
Widjaja, A. A., Singh, B. K., Adami, E., Viswanathan, S., Dong, J., D’Agostino, G. A., Ng, B., Lim, W., Tan, J., Paleja, B. S., et al. (2019) · Gastroenterology · doi:10.1053/j.gastro.2019.05.002 · Cited by 279
Reversibility of liver fibrosis
Sun, M., & Kisseleva, T. (2015) · Clinics and Research in Hepatology and Gastroenterology · doi:10.1016/j.clinre.2015.06.015 · Cited by 280
Cell fusion induced by ERVWE1 or measles virus causes cellular senescence
Chuprin, A., Gal, H., Biron-Shental, T., Biran, A., Amiel, A., Rozenblatt, S., & Krizhanovsky, V. (2013) · Genes & Development · doi:10.1101/gad.227512.113 · Cited by 262
Self-citationNuclear genomic instability and aging
Niedernhofer, L. J., Gurkar, A. U., Wang, Y., Vijg, J., Hoeijmakers, J. H. J., & Robbins, P. D. (2018) · Annual Review of Biochemistry · doi:10.1146/annurev-biochem-062917-012239 · Cited by 275
Dauch, D., Rudalska, R., Cossa, G., Nault, J., Kang, T.-W., Wüestefeld, T., Hohmeyer, A., Imbeaud, S., Yevsa, T., Hoenicke, L., et al. (2016) · Nature Medicine · doi:10.1038/nm.4107 · Cited by 280
Self-citationCellular and Molecular Mechanisms Underlying Liver Fibrosis Regression
Caligiuri, A., Gentilini, A., Pastore, M., Gitto, S., & Marra, F. (2021) · Cells · doi:10.3390/cells10102759 · Cited by 283
Bird, T. G., Müller, M., Boulter, L., Vincent, D. F., Ridgway, R. A., Lopez-Guadamillas, E., Lu, W.-Y., Jamieson, T., Govaere, O., Campbell, A. D., et al. (2018) · Science Translational Medicine · doi:10.1126/scitranslmed.aan1230 · Cited by 261
“SASP may also modulate fibrosis and regeneration in response to acute tissue injury (11, 16, 17).”
Cellular senescence and SASP in tumor progression and therapeutic opportunities
Dong, Z., Luo, Y., Yuan, Z., Tian, Y., Jin, T., & Feng, X. (2024) · Molecular Cancer · doi:10.1186/s12943-024-02096-7 · Cited by 315
Senescence-associated secretory phenotype contributes to pathological angiogenesis in retinopathy
Oubaha, M., Miloudi, K., Dejda, A., Guber, V., Mawambo, G., Germain, M.-A., Bourdel, G., Popovic, N., Rezende, F. A., Kaufman, R. J., et al. (2016) · Science Translational Medicine · doi:10.1126/scitranslmed.aaf9440 · Cited by 259
Increased PDGFRα Activation Disrupts Connective Tissue Development and Drives Systemic Fibrosis
Olson, L. E., & Soriano, P. (2009) · Developmental Cell · doi:10.1016/j.devcel.2008.12.003 · Cited by 264
Farr, J. N., & Khosla, S. (2019) · Bone · doi:10.1016/j.bone.2019.01.015 · Cited by 263
Kim, K.-H., Chen, C.-C., Monzon, R. I., & Lau, L. F. (2013) · Molecular and Cellular Biology · doi:10.1128/mcb.00049-13 · Cited by 261
Oxidative Stress in Pulmonary Fibrosis
Otoupalova, E., Smith, S., Cheng, G., & Thannickal, V. J. (2020) · Comprehensive physiology · doi:10.1002/cphy.c190017 · Cited by 312
Harnessing natural killer cells for cancer immunotherapy: dispatching the first responders
Maskalenko, N. A., Zhigarev, D. I., & Campbell, K. S. (2022) · Nature Reviews Drug Discovery · doi:10.1038/s41573-022-00413-7 · Cited by 265
Physiological and pathological consequences of cellular senescence
Burton, D. G. A., & Krizhanovsky, V. (2014) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-014-1691-3 · Cited by 253
Self-citationGeorgilis, A., Klotz, S., Hanley, C. J., Herranz, N., Weirich, B., Morancho, B., Leote, A. C., D'Artista, L., Gallage, S., Seehawer, M., et al. (2018) · Cancer Cell · doi:10.1016/j.ccell.2018.06.007 · Cited by 237
“Senescent hepatocytes are present in damaged livers (Jurk et al., 2014; Krizhanovsky et al., 2008), and during chronic liver disease precancerous senescent hepatocytes co-exist with readily transformed cells.”
Self-citationThe wound healing, chronic fibrosis, and cancer progression triad
Rybinski, B., Franco‐Barraza, J., & Cukierman, E. (2014) · Physiological Genomics · doi:10.1152/physiolgenomics.00158.2013 · Cited by 265
Cellular senescence controls fibrosis in wound healing
Jun, J.-I., & Lau, L. F. (2010) · Aging · doi:10.18632/aging.100201 · Cited by 255
Essential role for premature senescence of myofibroblasts in myocardial fibrosis
Meyer, K., Hodwin, B., Ramanujam, D., Engelhardt, S., & Sarikas, A. (2016) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2016.02.047 · Cited by 247
Untimely TGFβ responses in COVID-19 limit antiviral functions of NK cells
Witkowski, M., Tizian, C., Ferreira‐Gomes, M., Niemeyer, D., Jones, T. C., Heinrich, F., Frischbutter, S., Angermair, S., Hohnstein, T., Mattiola, I., et al. (2021) · Nature · doi:10.1038/s41586-021-04142-6 · Cited by 254
Van De Water, L., Varney, S., & Tomasek, J. J. (2013) · Advances in Wound Care · doi:10.1089/wound.2012.0393 · Cited by 251
Hoenicke, L., & Zender, L. (2012) · Carcinogenesis · doi:10.1093/carcin/bgs124 · Cited by 248
Self-citationMalaquin, N., Martinez, A., & Rodier, F. (2016) · Experimental Gerontology · doi:10.1016/j.exger.2016.05.010 · Cited by 247
Small molecule compounds that induce cellular senescence.
Petrova, N. V., Velichko, A. K., Razin, S. V., & Kantidze, O. L. (2016) · Aging Cell · doi:10.1111/acel.12518 · Cited by 240
“, 2013), the restriction of fibrosis (Krizhanovsky et al., 2008; Jun & Lau, 2010; Zhu et al., 2013), tissue repair (Demaria et al.”
BackgroundSestrins induce natural killer function in senescent-like CD8+ T cells
Pereira, B. I., Maeyer, R. P. H. D., Covre, L. P., Nehar-Belaid, D., Lanna, A., Ward, S., Marcheş, R., Chambers, E. S., Gomes, D. C. O., Riddell, N. E., et al. (2020) · Nature Immunology · doi:10.1038/s41590-020-0643-3 · Cited by 255
Natural killer cells in infection and inflammation of the lung
Culley, F. J. (2009) · Immunology · doi:10.1111/j.1365-2567.2009.03167.x · Cited by 253
Riegger, J., Schoppa, A., Ruths, L., Haffner‐Luntzer, M., & Ignatius, A. A. (2023) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-023-00489-y · Cited by 272
Granule exocytosis mediates immune surveillance of senescent cells
Sagiv, A., Biran, A., Yon, M., Simon, J., Lowe, S. W., & Krizhanovsky, V (2013) · Oncogene · doi:10.1038/onc.2012.206 · Cited by 240
Self-citationSenescent cells: SASPected drivers of age-related pathologies
Ovadya, Y., & Krizhanovsky, V. (2014) · Biogerontology · doi:10.1007/s10522-014-9529-9 · Cited by 232
Self-citation
Metadata
- Authors
- Krizhanovsky, V., Yon, M., Dickins, R. A., Hearn, S., Simon, J., Miething, C., Yee, H., Zender, L., & Lowe, S. W.
- Affiliations
- Cold Spring Harbor Laboratory (US)
- Universidade de São Paulo (BR)
- Howard Hughes Medical Institute (US)
- NYU Langone Health (US)
- Corresponding author
- Lowe, Scott W.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2008-10
- Volume
- 135
- Issue
- 1
- Pages
- 190
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3073300
- OpenAlex
- W1570233039
- Cited by
- 2,027
- References
- 34
- Citations by year
- 2026: 113 · 2025: 135 · 2024: 153 · 2023: 135 · 2022: 156 · 2021: 170 · 2020: 154 · 2019: 146 · 2018: 137 · 2017: 126 · 2016: 125 · 2015: 90 · 2014: 88 · 2013: 83 · 2012: 63
- FWCI
- 36.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1750 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Cold Spring Harbor Laboratory Institutional Repository (Cold Spring Harbor Laboratory) (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute on Aging (R56AG016379, AG-16379, R01AG016379)
- National Cancer Institute (P01CA013106, P30CA008748)
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Health Sciences › Medicine › Hepatology › Liver Disease Diagnosis and Treatment
- Keywords
- cellular senescence, activated hepatic stellate cells, liver fibrosis, liver cirrhosis, extracellular matrix deposition, natural killer cells, immune surveillance, cell cycle exit
- MeSH terms
- Animals, Carbon Tetrachloride, Cells, Cultured, Female, Fibroblasts, Humans, Killer Cells, Natural, Liver, Liver Cirrhosis, Liver Cirrhosis, Experimental, Cellular Senescence, Mice
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