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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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BackgroundThe types of hepatic myofibroblasts contributing to liver fibrosis of different etiologies
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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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