全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

S100A9在纤维化疾病中的研究进展
The Research Progress of S100A9 in Fibrotic Diseases

DOI: 10.12677/hjbm.2025.151023, PP. 198-206

Keywords: S100A9,纤维化,炎症
S100A9
, Fibrosis, Inflammation

Full-Text   Cite this paper   Add to My Lib

Abstract:

纤维化疾病是多种慢性疾病的终末阶段,其特点是组织中纤维结缔组织的过度积累,导致器官结构破坏和功能丧失。S100A9作为S100蛋白家族的重要成员,在多种炎症性疾病和癌症中的作用已被广泛研究,但其在纤维化疾病中的作用及机制尚未完全阐明。本文综述了S100A9在肺、肝、肾、心脏及皮肤等主要纤维化疾病中的研究进展,重点探讨其在细胞信号通路、免疫调节及炎症反应中的作用,旨在为纤维化疾病的诊断和治疗提供新的研究思路。
Fibrosis is the terminal stage of various chronic diseases, characterized by excessive accumulation of fibrous connective tissue in tissues, leading to organ structural damage and loss of function. As an important member of the S100 protein family, the role of S100A9 in various inflammatory diseases and cancers has been widely studied, but its role and mechanism in fibrotic diseases have not been fully elucidated. This article reviews the research progress of S100A9 in major fibrotic diseases such as lung, liver, kidney, heart, and skin, with a focus on exploring its role in cellular signaling pathways, immune regulation, and inflammatory response, aiming to provide new research ideas for the diagnosis and treatment of fibrotic diseases.

References

[1]  Maria, A.T.J., Bourgier, C., Martinaud, C., Borie, R., Rozier, P., Rivière, S., et al. (2020) De la fibrogenèse à la fibrose: Mécanismes physiopathologiques et présentations cliniques. La Revue de Médecine Interne, 41, 325-329.
https://doi.org/10.1016/j.revmed.2020.01.002
[2]  Piera-Velazquez, S., Mendoza, F. and Jimenez, S. (2016) Endothelial to Mesenchymal Transition (Endomt) in the Pathogenesis of Human Fibrotic Diseases. Journal of Clinical Medicine, 5, Article 45.
https://doi.org/10.3390/jcm5040045
[3]  Mack, M. (2018) Inflammation and Fibrosis. Matrix Biology, 68, 106-121.
https://doi.org/10.1016/j.matbio.2017.11.010
[4]  Meng, X., Nikolic-Paterson, D.J. and Lan, H.Y. (2014) Inflammatory Processes in Renal Fibrosis. Nature Reviews Nephrology, 10, 493-503.
https://doi.org/10.1038/nrneph.2014.114
[5]  Lafuse, W.P., Wozniak, D.J. and Rajaram, M.V.S. (2020) Role of Cardiac Macrophages on Cardiac Inflammation, Fibrosis and Tissue Repair. Cells, 10, Article 51.
https://doi.org/10.3390/cells10010051
[6]  Jha, J.C., Dai, A., Garzarella, J., Charlton, A., Urner, S., Østergaard, J.A., et al. (2022) Independent of Renox, NOX5 Promotes Renal Inflammation and Fibrosis in Diabetes by Activating Ros-Sensitive Pathways. Diabetes, 71, 1282-1298.
https://doi.org/10.2337/db21-1079
[7]  Schiopu, A. and Cotoi, O.S. (2013) S100A8 and S100A9: Damps at the Crossroads between Innate Immunity, Traditional Risk Factors, and Cardiovascular Disease. Mediators of Inflammation, 2013, 1-10.
https://doi.org/10.1155/2013/828354
[8]  Chen, B., Miller, A.L., Rebelatto, M., Brewah, Y., Rowe, D.C., Clarke, L., et al. (2015) S100A9 Induced Inflammatory Responses Are Mediated by Distinct Damage Associated Molecular Patterns (DAMP) Receptors in Vitro and in Vivo. PLOS ONE, 10, e0115828.
https://doi.org/10.1371/journal.pone.0115828
[9]  Zhong, A., Xu, W., Zhao, J., Xie, P., Jia, S., Sun, J., et al. (2016) S100A8 and S100A9 Are Induced by Decreased Hydration in the Epidermis and Promote Fibroblast Activation and Fibrosis in the Dermis. The American Journal of Pathology, 186, 109-122.
https://doi.org/10.1016/j.ajpath.2015.09.005
[10]  Moles, A., Murphy, L., Wilson, C.L., Chakraborty, J.B., Fox, C., Park, E.J., et al. (2014) A TLR2/S100A9/CXCL-2 Signaling Network Is Necessary for Neutrophil Recruitment in Acute and Chronic Liver Injury in the Mouse. Journal of Hepatology, 60, 782-791.
https://doi.org/10.1016/j.jhep.2013.12.005
[11]  Chen, H., Lunney, J.K., Cheng, L., Li, X., Cao, J., Zhu, M., et al. (2011) Porcine S100A8 and S100A9: Molecular Characterizations and Crucial Functions in Response to Haemophilus Parasuis Infection. Developmental & Comparative Immunology, 35, 490-500.
https://doi.org/10.1016/j.dci.2010.11.017
[12]  Tamulytė, R., Jankaitytė, E., Toleikis, Z., Smirnovas, V. and Jankunec, M. (2023) Pro-Inflammatory Protein S100A9 Alters Membrane Organization by Dispersing Ordered Domains. Biochimica et Biophysica Acta (BBA)—Biomembranes, 1865, Article 184113.
https://doi.org/10.1016/j.bbamem.2022.184113
[13]  Fan, Z.P., Peng, M.L., Chen, Y.Y., Xia, Y.Z., Liu, C.Y., Zhao, K., et al. (2021) S100A9 Activates the Immunosuppressive Switch through the PI3K/Akt Pathway to Maintain the Immune Suppression Function of Testicular Macrophages. Frontiers in Immunology, 12, Article 743354.
https://doi.org/10.3389/fimmu.2021.743354
[14]  Averill, M.M., Barnhart, S., Becker, L., Li, X., Heinecke, J.W., LeBoeuf, R.C., et al. (2011) S100A9 Differentially Modifies Phenotypic States of Neutrophils, Macrophages, and Dendritic Cells. Circulation, 123, 1216-1226.
https://doi.org/10.1161/circulationaha.110.985523
[15]  Simard, J., Girard, D. and Tessier, P.A. (2010) Induction of Neutrophil Degranulation by S100A9 via a MAPK-Dependent Mechanism. Journal of Leukocyte Biology, 87, 905-914.
https://doi.org/10.1189/jlb.1009676
[16]  Chi, Z., Hayasaka, Y., Zhang, X., Cui, H. and Hayasaka, S. (2007) S100a9-Positive Granulocytes and Monocytes in Lipopolysaccharide-Induced Anterior Ocular Inflammation. Experimental Eye Research, 84, 254-265.
https://doi.org/10.1016/j.exer.2006.09.016
[17]  Zhou, Y., Wu, M., Xu, L., Cheng, J., Shen, J., Yang, T., et al. (2021) Bmal1 Regulates Macrophage Polarize through Glycolytic Pathway in Alcoholic Liver Disease. Frontiers in Pharmacology, 12, Article 640521.
https://doi.org/10.3389/fphar.2021.640521
[18]  Cheng, P., Corzo, C.A., Luetteke, N., Yu, B., Nagaraj, S., Bui, M.M., et al. (2008) Inhibition of Dendritic Cell Differentiation and Accumulation of Myeloid-Derived Suppressor Cells in Cancer Is Regulated by S100A9 Protein. The Journal of Experimental Medicine, 205, 2235-2249.
https://doi.org/10.1084/jem.20080132
[19]  Mihaila, A.C., Ciortan, L., Macarie, R.D., Vadana, M., Cecoltan, S., Preda, M.B., et al. (2021) Transcriptional Profiling and Functional Analysis of N1/N2 Neutrophils Reveal an Immunomodulatory Effect of S100A9-Blockade on the Pro-Inflammatory N1 Subpopulation. Frontiers in Immunology, 12, Article 708770.
https://doi.org/10.3389/fimmu.2021.708770
[20]  Ursino, G., Lucibello, G., Teixeira, P.D.S., Höfler, A., Veyrat-Durebex, C., Odouard, S., et al. (2024) S100A9 Exerts Insulin-Independent Antidiabetic and Anti-Inflammatory Effects. Science Advances, 10, eadj4686.
https://doi.org/10.1126/sciadv.adj4686
[21]  Vogl, T., Stratis, A., Wixler, V., Völler, T., Thurainayagam, S., Jorch, S.K., et al. (2018) Autoinhibitory Regulation of S100A8/S100A9 Alarmin Activity Locally Restricts Sterile Inflammation. Journal of Clinical Investigation, 128, 1852-1866.
https://doi.org/10.1172/jci89867
[22]  Xu, Y., Wang, Y., Ning, K. and Bao, Y. (2024) Unraveling the Mechanisms of S100A8/A9 in Myocardial Injury and Dysfunction. Current Issues in Molecular Biology, 46, 9707-9720.
https://doi.org/10.3390/cimb46090577
[23]  Agra, R.M., Fernández-Trasancos, Á., Sierra, J., González-Juanatey, J.R. and Eiras, S. (2014) Differential Association of S100A9, an Inflammatory Marker, and P53, a Cell Cycle Marker, Expression with Epicardial Adipocyte Size in Patients with Cardiovascular Disease. Inflammation, 37, 1504-1512.
https://doi.org/10.1007/s10753-014-9876-3
[24]  Pei, H., Qu, J., Chen, J., Zhao, G. and Lu, Z. (2024) S100A9 as a Key Myocardial Injury Factor Interacting with ATP5 Exacerbates Mitochondrial Dysfunction and Oxidative Stress in Sepsis-Induced Cardiomyopathy. Journal of Inflammation Research, 17, 4483-4503.
https://doi.org/10.2147/jir.s457340
[25]  Pan, X., Yang, L., Wang, S., Liu, Y., Yue, L. and Chen, S. (2023) Semaglutide Ameliorates Obesity-Induced Cardiac Inflammation and Oxidative Stress Mediated via Reduction of Neutrophil Cxcl2, S100A8, and S100A9 Expression. Molecular and Cellular Biochemistry, 479, 1133-1147.
https://doi.org/10.1007/s11010-023-04784-2
[26]  Chang, N., Liu, Y., Li, W., Ma, Y., Zhou, X., Zhao, X., et al. (2024) Neutrophil-Secreted S100A8/A9 Participates in Fatty Liver Injury and Fibrosis by Promoting Myofibroblast Migration. Journal of Molecular Medicine, 102, 1117-1133.
https://doi.org/10.1007/s00109-024-02469-x
[27]  Du, L., Chen, Y., Shi, J., Yu, X., Zhou, J., Wang, X., et al. (2023) Inhibition of S100A8/A9 Ameliorates Renal Interstitial Fibrosis in Diabetic Nephropathy. Metabolism, 144, Article 155376.
https://doi.org/10.1016/j.metabol.2022.155376
[28]  Tammaro, A., Florquin, S., Brok, M., Claessen, N., Butter, L.M., Teske, G.J.D., et al. (2018) S100A8/A9 Promotes Parenchymal Damage and Renal Fibrosis in Obstructive Nephropathy. Clinical and Experimental Immunology, 193, 361-375.
https://doi.org/10.1111/cei.13154
[29]  Hou, C., Wang, D., Zhao, M., Ballar, P., Zhang, X., Mei, Q., et al. (2023) MANF Brakes TLR4 Signaling by Competitively Binding S100A8 with S100A9 to Regulate Macrophage Phenotypes in Hepatic Fibrosis. Acta Pharmaceutica Sinica B, 13, 4234-4252.
https://doi.org/10.1016/j.apsb.2023.07.027
[30]  Kang, J.H., Hwang, S.M. and Chung, I.Y. (2014) S100A8, S100A9 and S100A12 Activate Airway Epithelial Cells to Produce MUC5AC via Extracellular Signal-Regulated Kinase and Nuclear Factor-κB Pathways. Immunology, 144, 79-90.
https://doi.org/10.1111/imm.12352
[31]  Halayko, A.J. and Ghavami, S. (2009) S100A8/A9: A Mediator of Severe Asthma Pathogenesis and Morbidity? Canadian Journal of Physiology and Pharmacology, 87, 743-755.
https://doi.org/10.1139/y09-054
[32]  Xu, X., Chen, H., Zhu, X., Ma, Y., Liu, Q., Xue, Y., et al. (2013) S100A9 Promotes Human Lung Fibroblast Cells Activation through Receptor for Advanced Glycation End-Product-Mediated Extracellular-Regulated Kinase 1/2, Mitogen-Activated Protein-Kinase and Nuclear Factor-κB-Dependent Pathways. Clinical and Experimental Immunology, 173, 523-535.
https://doi.org/10.1111/cei.12139
[33]  Xu, X., et al. (2018) S100A9 Aggravates Bleomycin-Induced Dermal Fibrosis in Mice via Activation of ERK1/2 MAPK and NF-κB Pathways. Iranian Journal of Basic Medical Sciences, 21, 194-201.
[34]  Araki, K., Kinoshita, R., Tomonobu, N., Gohara, Y., Tomida, S., Takahashi, Y., et al. (2020) The Heterodimer S100A8/A9 Is a Potent Therapeutic Target for Idiopathic Pulmonary Fibrosis. Journal of Molecular Medicine, 99, 131-145.
https://doi.org/10.1007/s00109-020-02001-x
[35]  Park, E.Y., Seo, M.J. and Park, J.H. (2010) Effects of Specific Genes Activating RAGE on Polycystic Kidney Disease. American Journal of Nephrology, 32, 169-178.
https://doi.org/10.1159/000315859
[36]  Dessing, M.C., Tammaro, A., Pulskens, W.P., Teske, G.J., Butter, L.M., Claessen, N., et al. (2015) The Calcium-Binding Protein Complex S100A8/A9 Has a Crucial Role in Controlling Macrophage-Mediated Renal Repair Following Ischemia/Reperfusion. Kidney International, 87, 85-94.
https://doi.org/10.1038/ki.2014.216
[37]  Yao, W., Chen, Y., Li, Z., Ji, J., You, A., Jin, S., et al. (2022) Single Cell RNA Sequencing Identifies a Unique Inflammatory Macrophage Subset as a Druggable Target for Alleviating Acute Kidney Injury. Advanced Science, 9, Article 2103675.
https://doi.org/10.1002/advs.202103675
[38]  Liu, J., Chen, X., Zeng, L., Zhang, L., Wang, F., Peng, C., et al. (2024) Targeting S100A9 Prevents Β-Adrenergic Activation-Induced Cardiac Injury. Inflammation, 47, 789-806.
https://doi.org/10.1007/s10753-023-01944-w
[39]  Shen, S., Zhang, M., Wang, X., Liu, Q., Su, H., Sun, B., et al. (2024) Single-Cell RNA Sequencing Reveals S100A9HI Macrophages Promote the Transition from Acute Inflammation to Fibrotic Remodeling after Myocardial Ischemia-Reperfusion. Theranostics, 14, 1241-1259.
https://doi.org/10.7150/thno.91180
[40]  Boyd, J.H., Kan, B., Roberts, H., Wang, Y. and Walley, K.R. (2008) S100A8 and S100A9 Mediate Endotoxin-Induced Cardiomyocyte Dysfunction via the Receptor for Advanced Glycation End Products. Circulation Research, 102, 1239-1246.
https://doi.org/10.1161/circresaha.107.167544
[41]  Marinković, G., Grauen Larsen, H., Yndigegn, T., Szabo, I.A., Mares, R.G., de Camp, L., et al. (2019) Inhibition of Pro-Inflammatory Myeloid Cell Responses by Short-Term S100A9 Blockade Improves Cardiac Function after Myocardial Infarction. European Heart Journal, 40, 2713-2723.
https://doi.org/10.1093/eurheartj/ehz461
[42]  Marinković, G., Koenis, D.S., de Camp, L., Jablonowski, R., Graber, N., de Waard, V., et al. (2020) S100A9 Links Inflammation and Repair in Myocardial Infarction. Circulation Research, 127, 664-676.
https://doi.org/10.1161/circresaha.120.315865
[43]  Müller, I., Vogl, T., Kühl, U., Krannich, A., Banks, A., Trippel, T., et al. (2020) Serum Alarmin S100A8/S100A9 Levels and Its Potential Role as Biomarker in Myocarditis. ESC Heart Failure, 7, 1442-1451.
https://doi.org/10.1002/ehf2.12760
[44]  Sun, Y., Wang, Z., Wang, C., Tang, Z. and Zhao, H. (2021) Psycho-Cardiology Therapeutic Effects of Shuangxinfang in Rats with Depression-Behavior Post Acute Myocardial Infarction: Focus on Protein S100A9 from Proteomics. Biomedicine & Pharmacotherapy, 144, Article 112303.
https://doi.org/10.1016/j.biopha.2021.112303
[45]  Chalise, U., Becirovic-Agic, M., Daseke, M.J., Konfrst, S.R., Rodriguez-Paar, J.R., Feng, D., et al. (2022) S100A9 Is a Functional Effector of Infarct Wall Thinning after Myocardial Infarction. American Journal of Physiology-Heart and Circulatory Physiology, 322, H145-H155.
https://doi.org/10.1152/ajpheart.00475.2021
[46]  Feng, L., Li, G., An, J., Liu, C., Zhu, X., Xu, Y., et al. (2022) Exercise Training Protects against Heart Failure via Expansion of Myeloid-Derived Suppressor Cells through Regulating IL-10/STAT3/S100A9 Pathway. Circulation: Heart Failure, 15, e008550.
https://doi.org/10.1161/circheartfailure.121.008550
[47]  Meng, L., Wang, J., Chen, H., Zhu, J., Kong, F., Chen, G., et al. (2024) LncRNA MEG9 Promotes Inflammation and Liver Fibrosis through S100A9 in Biliary Atresia. Journal of Pediatric Surgery, 60, Article 161633.
https://doi.org/10.1016/j.jpedsurg.2024.07.018
[48]  de Ponti, A., Wiechert, L., Stojanovic, A., Longerich, T., Marhenke, S., Hogg, N., et al. (2014) Chronic Liver Inflammation and Hepatocellular Carcinogenesis Are Independent of S100A9. International Journal of Cancer, 136, 2458-2463.
https://doi.org/10.1002/ijc.29282
[49]  Bouloukaki, I., Michelakis, S., Tsitoura, E., Vasarmidi, E., Koutoulaki, C., Tzanakis, N., et al. (2024) KL‑6, ET‑1 and S100A9 Levels in Patients with Idiopathic Pulmonary Fibrosis and Obstructive Sleep Apnea. Experimental and Therapeutic Medicine, 29, Article No. 16.
https://doi.org/10.3892/etm.2024.12766
[50]  Yamashita, M., Utsumi, Y., Nagashima, H., Nitanai, H. and Yamauchi, K. (2021) S100A9/CD163 Expression Profiles in Classical Monocytes as Biomarkers to Discriminate Idiopathic Pulmonary Fibrosis from Idiopathic Nonspecific Interstitial Pneumonia. Scientific Reports, 11, Article No. 12135.
https://doi.org/10.1038/s41598-021-91407-9
[51]  Lee, J., Kim, M.K., Kim, M., Lee, S.J., Park, S., Chang, H.S., et al. (2024) S100 Calcium-Binding Protein A9, a Potential Novel Diagnostic Biomarker for Idiopathic Pulmonary Fibrosis. Journal of Korean Medical Science, 39, e13.
https://doi.org/10.3346/jkms.2024.39.e13
[52]  Tanaka, K., Enomoto, N., Hozumi, H., Isayama, T., Naoi, H., Aono, Y., et al. (2021) Serum S100A8 and S100A9 as Prognostic Biomarkers in Acute Exacerbation of Idiopathic Pulmonary Fibrosis. Respiratory Investigation, 59, 827-836.
https://doi.org/10.1016/j.resinv.2021.05.008
[53]  Bargagli, E., Olivieri, C., Cintorino, M., Refini, R.M., Bianchi, N., Prasse, A., et al. (2010) Calgranulin B (S100A9/MRP14): A Key Molecule in Idiopathic Pulmonary Fibrosis? Inflammation, 34, 85-91.
https://doi.org/10.1007/s10753-010-9210-7
[54]  Nikitorowicz-Buniak, J., Shiwen, X., Denton, C.P., Abraham, D. and Stratton, R. (2014) Abnormally Differentiating Keratinocytes in the Epidermis of Systemic Sclerosis Patients Show Enhanced Secretion of CCN2 and S100A9. Journal of Investigative Dermatology, 134, 2693-2702.
https://doi.org/10.1038/jid.2014.253
[55]  Stenström, M., Nyhlén, H.C., Törngren, M., Liberg, D., Sparre, B., Tuvesson, H., et al. (2016) Paquinimod Reduces Skin Fibrosis in Tight Skin 1 Mice, an Experimental Model of Systemic Sclerosis. Journal of Dermatological Science, 83, 52-59.
https://doi.org/10.1016/j.jdermsci.2016.04.006
[56]  Zhu, Z., Ni, S., Zhang, J., Yuan, Y., Bai, Y., Yin, X., et al. (2023) Genome-Wide Analysis of Dysregulated RNA-Binding Proteins and Alternative Splicing Genes in Keloid. Frontiers in Genetics, 14, Article 1118999.
https://doi.org/10.3389/fgene.2023.1118999
[57]  Hesselstrand, R., Distler, J.H.W., Riemekasten, G., Wuttge, D.M., Törngren, M., Nyhlén, H.C., et al. (2021) An Open-Label Study to Evaluate Biomarkers and Safety in Systemic Sclerosis Patients Treated with Paquinimod. Arthritis Research & Therapy, 23, Article 204.
https://doi.org/10.1186/s13075-021-02573-0
[58]  Miura, S., Iwamoto, H., Namba, M., Yamaguchi, K., Sakamoto, S., Horimasu, Y., et al. (2024) High S100A9 Level Predicts Poor Survival, and the S100A9 Inhibitor Paquinimod Is a Candidate for Treating Idiopathic Pulmonary Fibrosis. BMJ Open Respiratory Research, 11, e001803.
https://doi.org/10.1136/bmjresp-2023-001803

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133