Interleukin-22 induces hepatic stellate cell senescence and restricts liver fibrosis in mice
Open accessAbstract
Interleukin (IL)-22 is known to play a key role in promoting antimicrobial immunity, inflammation, and tissue repair at barrier surfaces by binding to the receptors, IL-10R2 and IL-22R1. IL-22R1 is generally thought to be expressed exclusively in epithelial cells. In this study, we identified high levels of IL-10R2 and IL-22R1 expression on hepatic stellate cells (HSCs), the predominant cell type involved in liver fibrogenesis in response to liver damage. In vitro treatment with IL-22 induced the activation of signal transducer and activator of transcription (STAT) 3 in primary mouse and human HSCs. IL-22 administration prevented HSC apoptosis in vitro and in vivo , but surprisingly, the overexpression of IL-22 by either gene targeting (e.g., IL-22 transgenic mice) or exogenous administration of adenovirus expressing IL-22 reduced liver fibrosis and accelerated the resolution of liver fibrosis during recovery. Furthermore, IL-22 overexpression or treatment increased the number of senescence-associated beta-galactosidase-positive HSCs and decreased alpha-smooth muscle actin expression in fibrotic livers in vivo and cultured HSCs in vitro . Deletion of STAT3 prevented IL-22-induced HSC senescence in vitro , whereas the overexpression of a constitutively activated form of STAT3 promoted HSC senescence through p53- and p21-dependent pathways. Finally, IL-22 treatment up-regulated the suppressor of cytokine signaling (SOCS) 3 expression in HSCs. Immunoprecipitation analyses revealed that SOCS3 bound p53 and subsequently increased the expression of p53 and its target genes, contributing to IL-22-mediated HSC senescence. Conclusion : IL-22 induces the senescence of HSCs, which express both IL-10R2 and IL-22R1, thereby ameliorating liver fibrogenesis. The antifibrotic effect of IL-22 is likely mediated by the induction of HSC senescence, in addition to the previously discovered hepatoprotective functions of IL-22.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Previous studies detected elevated STAT3 phosphorylation in all rodent models with liver injury and fibrosis and in samples of patients with fibrosis and cirrhosis.
“Previous studies detected elevated STAT3 phosphorylation in all rodent models with liver injury and fibrosis and in the samples of patients with fibrosis and cirrhosis [46, 47].”
From Saikosaponin b1 Attenuates Liver Fibrosis by Blocking STAT3/Gli1 Interaction and Inducing Gli1 Degradation (2025) · cites this paper as [47]
The Results section on IL-22 signaling reports STAT3 activation after IL-22 exposure in cultured hepatic stellate cells. The Animal models section describes a mouse fibrosis model, but neither passage reports elevated STAT3 phosphorylation across rodent injury models or in patient samples with fibrosis or cirrhosis. Searches for those specific observations found no supporting passage in our copy; page numbers were unavailable. (LLM, conf=0.76)
Experimental — accuracy not yet measuredThere is evidence of a beneficial effect of both pro-senescent and anti-senescent approaches, depending on context.
“There is evidence of a beneficial effect of both pro-senescent and anti-senescent approaches, depending on context.”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [300]
A pro-senescent effect may be desirable in treating cancer, renal, liver and cutaneous fibrosis.
“A pro-senescent effect may be desirable in treating cancer [295,296,297], renal, liver and cutaneous fibrosis [298,299,300,301].”
From Ageing, Cellular Senescence and Neurodegenerative Disease (2018) · cites this paper as [300]
IL-22, which is produced by ILC3 and signals through the IL-22/IL-22R1/IL-10R2 complex, ameliorated experimental liver fibrosis by inducing HSC senescence via upregulation of STAT3.
“Accordingly, IL-22, which is produced by ILC3 and signals through the IL-22/IL-22R1/IL-10R2 complex, ameliorated experimental liver fibrosis by inducing HSC senescence via upregulation of STAT3.91”
From Understanding the cellular interactome of non-alcoholic fatty liver disease (2022) · cites this paper as [91]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Cites
Bataller, R., & Brenner, D. A. (2005) · Journal of Clinical Investigation · doi:10.1172/jci24282 · Cited by 4,958 · see citing works
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 · see citing works
Hepatic Stellate Cells: Protean, Multifunctional, and Enigmatic Cells of the Liver
Friedman, S. L. (2008) · Physiological Reviews · doi:10.1152/physrev.00013.2007 · Cited by 2,842 · see citing works
Mechanisms of Hepatic Fibrogenesis
Friedman, S. L. (2008) · Gastroenterology · doi:10.1053/j.gastro.2008.03.003 · Cited by 2,640 · see citing works
Oncogene-Induced Senescence Relayed by an Interleukin-Dependent Inflammatory Network
Kuilman, T., Michaloglou, C., Vredeveld, L. C. W., Douma, S., van Doorn, R., Desmet, C. J., Aarden, L. A., Mooi, W. J., & Peeper, D. S. (2008) · Cell · doi:10.1016/j.cell.2008.03.039 · Cited by 2,086 · see citing works
Senescence of activated stellate cells limits liver fibrosis
Krizhanovsky, V., Yon, M., Dickins, R. A., Hearn, S., Simon, J., Miething, C., Yee, H., Zender, L., & Lowe, S. W. (2008) · Cell · doi:10.1016/j.cell.2008.06.049 · Cited by 2,029 · see citing works
Senescence of Activated Stellate Cells Limits Liver Fibrosis
Krizhanovsky, V., Yon, M., Dickins, R. A., Hearn, S., Simon, J., Miething, C., Yee, H., Zender, L., & Lowe, S. W. (2008) · Cell · doi:10.1016/j.cell.2008.09.015 · Cited by 2,027
Chemokine signaling via the CXCR2 receptor reinforces senescence
Acosta, J. C., O'Loghlen, A., Banito, A., Guijarro, M. V., Augert, A., Raguz, S., Fumagalli, M., Da Costa, M., Brown, C., Popov, N., et al. (2008) · Cell · doi:10.1016/j.cell.2008.03.038 · Cited by 1,801 · see citing works
The Biological Functions of T Helper 17 Cell Effector Cytokines in Inflammation
Ouyang, W., Kolls, J. K., & Zheng, Y. (2008) · Immunity · doi:10.1016/j.immuni.2008.03.004 · Cited by 1,697 · see citing works
Sonnenberg, G. F., Fouser, L., & Artis, D. (2011) · Nature Immunology · doi:10.1038/ni.2025 · Cited by 1,067 · see citing works
Radaeva, S., Sun, R., Pan, H., Hong, F., & Gao, B. (2004) · Hepatology · doi:10.1002/hep.20184 · Cited by 638 · see citing works
Self-citationA novel role for high-mobility group A proteins in cellular senescence and heterochromatin formation
Narita, M., Narita, M., Krizhanovsky, V., Nuñez, S., Chicas, A., Hearn, S. A., Myers, M. P., & Lowe, S. W. (2006) · Cell · doi:10.1016/j.cell.2006.05.052 · Cited by 629 · see citing works
Zenewicz, L. A., Yancopoulos, G. D., Valenzuela, D. M., Murphy, A. J., Karow, M. L., & Flavell, R. A. (2007) · Immunity · doi:10.1016/j.immuni.2007.07.023 · Cited by 628 · see citing works
Hepatocyte growth factor gene therapy of liver cirrhosis in rats
植木, 孝., Kaneda, Y., Tsutsui, H., Nakanishi, K., Sawa, Y., Morishita, R., Matsumoto, K., Nakamura, T., Takahashi, H., Okamoto, E., et al. (1999) · Nature Medicine · doi:10.1038/5593 · Cited by 588 · see citing works
Andoh, A., Zhang, Z., Inatomi, O., Fujino, S., Deguchi, Y., Araki, Y., Tsujikawa, T., Kitoh, K., Kim‐Mitsuyama, S., Takayanagi, A., et al. (2005) · Gastroenterology · doi:10.1053/j.gastro.2005.06.071 · Cited by 480 · see citing works
Phosphorylation of p53 Serine 15 Increases Interaction with CBP
Lambert, P. F., Kashanchi, F., Radonovich, M. F., Shiekhattar, R., & Brady, J. N. (1998) · Journal of Biological Chemistry · doi:10.1074/jbc.273.49.33048 · Cited by 423 · see citing works
Wolk, K., Witte, E., Witte, K., Warszawska, K., & Sabat, R. (2010) · Seminars in Immunopathology · doi:10.1007/s00281-009-0188-x · Cited by 395 · see citing works
Asahina, K., Zhou, B., Pu, W. T., & Tsukamoto, H. (2010) · Hepatology · doi:10.1002/hep.24119 · Cited by 308 · see citing works
Oncogenic <i>ras</i> and p53 Cooperate To Induce Cellular Senescence
Ferbeyre, G., de Stanchina, E., Lin, A. W., Querido, E., McCurrach, M. E., Hannon, G. J., & Lowe, S. W. (2002) · Molecular and Cellular Biology · doi:10.1128/mcb.22.10.3497-3508.2002 · Cited by 290 · see citing works
Park, O., Wang, H., Weng, H., Feigenbaum, L., Li, H., Yin, S., Ki, S. H., Yoo, S. H., Dooley, S., Wang, F., et al. (2011) · Hepatology · doi:10.1002/hep.24339 · Cited by 242 · see citing works
Self-citationSchnabl, B., Purbeck, C. A., Choi, Y. H., Hagedorn, C. H., & Brenner, D. (2003) · Hepatology · doi:10.1053/jhep.2003.50097 · Cited by 224 · see citing works
Tumour suppression by p53: the importance of apoptosis and cellular senescence
Zuckerman, V., Wolyniec, K., Sionov, R. V., Haupt, S., & Haupt, Y. (2009) · The Journal of Pathology · doi:10.1002/path.2584 · Cited by 210 · see citing works
A Proinflammatory Role for Interleukin-22 in the Immune Response to Hepatitis B Virus
Zhang, Y., Cobleigh, M. A., Lian, J., Huang, C., Booth, C. J., Bai, X., & Robek, M. D. (2011) · Gastroenterology · doi:10.1053/j.gastro.2011.06.051 · Cited by 161 · see citing works
SOCS1 Links Cytokine Signaling to p53 and Senescence
Calabrese, V., Mallette, F. A., Deschênes‐Simard, X., Ramanathan, S., Gagnon, J., Moores, A., Ilangumaran, S., & Ferbeyre, G. (2009) · Molecular Cell · doi:10.1016/j.molcel.2009.09.044 · Cited by 141 · see citing works
Hampel, B., Wagner, M., Teis, D., Zwerschke, W., Huber, L. A., & Jansen‐Dürr, P. (2005) · Aging Cell · doi:10.1111/j.1474-9726.2005.00180.x · Cited by 70 · see citing works
IL‐22 and non‐ELR‐CXC chemokine expression in chronic hepatitis B virus‐infected liver
Xiang, X., Gui, H., King, N. J. C., Cole, L., Wang, H., Xie, Q., & Bao, S. (2011) · Immunology and Cell Biology · doi:10.1038/icb.2011.79 · Cited by 65 · see citing works
Self-citationSOCS3 regulates p21 expression and cell cycle arrest in response to DNA damage
Sitko, J. C., Yeh, B. K., Kim, M., Zhou, H., Takaesu, G., Yoshimura, A., McBride, W. H., Jewett, A., Jamieson, C. A. M., & Cacalano, N. A. (2008) · Cellular Signalling · doi:10.1016/j.cellsig.2008.08.011 · Cited by 41 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Cellular senescence: from physiology to pathology
Muñoz-Espín, D., & Serrano, M. (2014) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3823 · Cited by 2,818 · see citing works
Cellular senescence in aging and age-related disease: from mechanisms to therapy
Childs, B. G., Durik, M., Baker, D. J., & van Deursen, J. M. (2015) · Nature Medicine · doi:10.1038/nm.4000 · Cited by 2,363 · see citing works
Cellular Senescence: Aging, Cancer, and Injury
Calcinotto, A., Kohli, J., Zagato, E., Pellegrini, L., Demaria, M., & Alimonti, A. (2019) · Physiological Reviews · doi:10.1152/physrev.00020.2018 · Cited by 1,270 · see citing works
Hepatic inflammation and fibrosis: Functional links and key pathways
Seki, E., & Schwabe, R. F. (2015) · Hepatology · doi:10.1002/hep.27332 · Cited by 972 · see citing works
Hepatic inflammatory responses in liver fibrosis
Hammerich, L., & Tacke, F. (2023) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-023-00807-x · Cited by 803 · see citing works
Non-Cell-Autonomous Tumor Suppression by p53
Lujambio, A., Akkari, L., Simon, J., Grace, D., Tschaharganeh, D. F., Bolden, J. E., Zhao, Z., Thapar, V., Joyce, J. A., Krizhanovsky, V., et al. (2013) · Cell · doi:10.1016/j.cell.2013.03.020 · Cited by 766 · see citing works
“In the context of certain wound-healing responses, SASP limits the extent of tissue damage and facilitates wound resolution (Kong et al., 2012; Krizhanovsky et al., 2008).”
BackgroundPathogenesis of alcoholic liver disease: Role of oxidative metabolism
Ceni, E., Mello, T., & Galli, A. (2014) · World Journal of Gastroenterology · doi:10.3748/wjg.v20.i47.17756 · Cited by 521 · see citing works
Ageing, Cellular Senescence and Neurodegenerative Disease
Kritsilis, M., V. Rizou, S., Koutsoudaki, P. N., Evangelou, K., Gorgoulis, V. G., & Papadopoulos, D. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19102937 · Cited by 448 · see citing works
Pathophysiological Aspects of Alcohol Metabolism in the Liver
Hyun, J., Han, J., Lee, C., Yoon, M., & Jung, Y. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22115717 · Cited by 324 · see citing works
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 · see citing works
“SASP may also modulate fibrosis and regeneration in response to acute tissue injury (11, 16, 17).”
Cellular mechanisms of tissue fibrosis. 5. Novel insights into liver fibrosis
Mallat, A., & Lotersztajn, S. (2013) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00230.2013 · Cited by 211 · see citing works
The Role of Innate Immune Cells in Nonalcoholic Steatohepatitis
Cai, J., Zhang, X., & Li, H. (2019) · Hepatology · doi:10.1002/hep.30506 · Cited by 207 · see citing works
Hepatic fibrosis: It is time to go with hepatic stellate cell-specific therapeutic targets
Ezhilarasan, D., Sokal, E., & Najimi, M. (2018) · Hepatobiliary & Pancreatic Diseases International · doi:10.1016/j.hbpd.2018.04.003 · Cited by 204 · see citing works
The role of growth hormone and insulin-like growth factor-I in the liver
Takahashi, Y. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18071447 · Cited by 193 · see citing works
Kwon, H.-J., Won, Y.-S., Park, O., Chang, B., Duryee, M. J., Thiele, G. E., Matsumoto, A., Singh, S., Abdelmegeed, M. A., Song, B.-J., et al. (2014) · Hepatology · doi:10.1002/hep.27036 · Cited by 191 · see citing works
Self-citationHammerich, L., Bangen, J. M., Govaere, O., Zimmermann, H. W., Gassler, N., Huss, S., Liedtke, C., Prinz, I., Lira, S. A., Luedde, T., et al. (2014) · Hepatology · doi:10.1002/hep.26697 · Cited by 190 · see citing works
IL-6-STAT3 signaling and premature senescence
Kojima, H., Inoue, T., Kunimoto, H., & Nakajima, K. (2013) · JAK-STAT · doi:10.4161/jkst.25763 · Cited by 170 · see citing works
IL-22 promotes fibroblast-mediated wound repair in the skin
McGee, H. M., Schmidt, B. A., Booth, C. J., Yancopoulos, G. D., Valenzuela, D. M., Murphy, A. J., Stevens, S., Flavell, R. A., & Horsley, V. (2013) · Journal of Investigative Dermatology · doi:10.1038/jid.2012.463 · Cited by 161 · see citing works
Type 3 cytokines IL-17A and IL-22 drive TGF-β–dependent liver fibrosis
Fabre, T., Molina, M. F., Soucy, G., Goulet, J.-P., Willems, B., Villeneuve, J.-P., Bilodeau, M., & Shoukry, N. H. (2018) · Science Immunology · doi:10.1126/sciimmunol.aar7754 · Cited by 155 · see citing works
Lozano-Torres, B., Estepa-Fernández, A., Rovira, M., Orzáez, M., Serrano, M., Martínez-Máñez, R., & Sancenón, F. (2019) · Nature Reviews Chemistry · doi:10.1038/s41570-019-0108-0 · Cited by 140 · see citing works
Understanding the cellular interactome of non-alcoholic fatty liver disease
Wallace, S. J., Tacke, F., Schwabe, R. F., & Henderson, N. C. (2022) · JHEP Reports · doi:10.1016/j.jhepr.2022.100524 · Cited by 116 · see citing works
Cell senescence in liver diseases: pathological mechanism and theranostic opportunity
Sanfeliu-Redondo, D., Gibert-Ramos, A., & Gracia-Sancho, J. (2024) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/s41575-024-00913-4 · Cited by 117 · see citing works
Zhang, Z., Yao, Z., Zhao, S., Shao, J., Chen, A., Zhang, F., & Zheng, S. (2017) · Cell Death & Disease · doi:10.1038/cddis.2017.255 · Cited by 97 · see citing works
Huang, Y.-H., Chen, M.-H., Guo, Q.-L., Chen, Z.-X., Chen, Q.-D., & Wang, X.-Z. (2020) · Cellular Signalling · doi:10.1016/j.cellsig.2019.109445 · Cited by 90 · see citing works
Short-term gain, long-term pain: the senescence life cycle and cancer
Chan, A. S. L., & Narita, M. (2019) · Genes & Development · doi:10.1101/gad.320937.118 · Cited by 80 · see citing works
MicroRNA controls of cellular senescence
Suh, N. (2018) · BMB Reports · doi:10.5483/bmbrep.2018.51.10.209 · Cited by 78 · see citing works
Targeting senescent cells improves functional recovery after spinal cord injury
Paramos-de-Carvalho, D., Martins, I., Cristóvão, A. M., Dias, A. F., Neves-Silva, D., Pereira, T., Chapela, D., Farinho, A., Jacinto, A., & Saúde, L. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109334 · Cited by 74 · see citing works
STAT3 in hepatocellular carcinoma: new perspectives
Svinka, J., Mikulits, W., & Eferl, R. (2014) · Hepatic Oncology · doi:10.2217/hep.13.7 · Cited by 63 · see citing works
The Origin and Fate of Liver Myofibroblasts
Kim, H. Y., Sakane, S., Eguileor, A., Carvalho Gontijo Weber, R., Lee, W., Liu, X., Lam, K., Ishizuka, K., Rosenthal, S. B., Diggle, K., et al. (2024) · Cellular and Molecular Gastroenterology and Hepatology · doi:10.1016/j.jcmgh.2023.09.008 · Cited by 63 · see citing works
Su, S.-B., Qin, S.-Y., Xian, X.-L., Huang, F.-F., Huang, Q.-L., ZhangDi, H.-J., & Jiang, H.-X. (2021) · Life Sciences · doi:10.1016/j.lfs.2020.118677 · Cited by 40 · see citing works
Senescent cells enhance newt limb regeneration by promoting muscle dedifferentiation
Walters, H. E., Troyanovskiy, K. E., Graf, A. M., & Yun, M. H. (2023) · Aging Cell · doi:10.1111/acel.13826 · Cited by 39 · see citing works
The role of <scp>IL</scp>‐22 in the resolution of sterile and nonsterile inflammation
Alabbas, S. Y., Begun, J., Florin, T. H., & Oancea, I. (2018) · Clinical & Translational Immunology · doi:10.1002/cti2.1017 · Cited by 37 · see citing works
Guillot, A., Gasmi, I., Brouillet, A., Ait‐Ahmed, Y., Calderaro, J., Ruiz, I., Gao, B., Lotersztajn, S., Pawlotsky, J., & Lafdil, F. (2018) · Hepatology Communications · doi:10.1002/hep4.1145 · Cited by 38 · see citing works
Self-citationCrosstalk between NK cells and hepatic stellate cells in liver fibrosis (Review)
Zhang, Y., Wu, Y., Shen, W., Wang, B., & Yuan, X. (2022) · Molecular Medicine Reports · doi:10.3892/mmr.2022.12724 · Cited by 35 · see citing works
Mechanisms of liver fibrosis in metabolic syndrome
Mehal, W. (2023) · eGastroenterology · doi:10.1136/egastro-2023-100015 · Cited by 28 · see citing works
Shao, M., Zhang, X., Sun, J., Dong, H., Han, X., Yang, Q., Chen, R., Shen, L., Xu, L., Wang, L., et al. (2025) · Exploration · doi:10.1002/exp.70000 · Cited by 26 · see citing works
Out with the old, in with the new: senescence in development
Czarkwiani, A., & Yun, M. H. (2018) · Current Opinion in Cell Biology · doi:10.1016/j.ceb.2018.05.014 · Cited by 24 · see citing works
Innate lymphoid cell-derived cytokines in autoimmune diseases
Li, S., Yang, D., Peng, T., Wu, Y., Tian, Z., & Ni, B. (2017) · Journal of Autoimmunity · doi:10.1016/j.jaut.2017.05.001 · Cited by 19 · see citing works
- Authors
- Kong, X., Feng, D., Wang, H., Hong, F., Bertola, A., Wang, F.-S., & Gao, B.
- Affiliations
- National Institutes of Health (US)
- Icahn School of Medicine at Mount Sinai (US)
- Corresponding author
- Gao, Bin
- Venue
- Hepatology
- Published
- 2012-09
- Volume
- 56
- Issue
- 3
- Pages
- 1150-1159
- ISSN
- 0270-9139 (ISSN-L)
- PMC
- PMC3394879
- OpenAlex
- W2079241145
- Cited by
- 448
- References
- 27
- Citations by year
- 2026: 16 · 2025: 31 · 2024: 39 · 2023: 36 · 2022: 23 · 2021: 35 · 2020: 38 · 2019: 25 · 2018: 44 · 2017: 30 · 2016: 33 · 2015: 32 · 2014: 33 · 2013: 24 · 2012: 8
- FWCI
- 19.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Hepatology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- Louisiana State University
- Hokkaido University
- National Institutes of Health (Z99‐AA999999)
- National Institute on Alcohol Abuse and Alcoholism (ZIAAA000368, ZIAAA000369)
- National Cancer Institute
- Topics
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Keywords
- IL-22, hepatic stellate cells, cellular senescence, liver fibrosis, STAT3 signaling, p53, p21, SOCS3, IL-10R2, antifibrotic therapy, alpha-smooth muscle actin, senescence-associated β-galactosidase
- MeSH terms
- Interleukin-22, Animals, Humans, Interleukins, Liver Cirrhosis, Mice, Inbred C57BL, Cellular Senescence, Mice, Hepatic Stellate Cells
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
