Journal of Cell Communication and Signaling最新文献

{"title":"Insights into the mediation of Ca2+ signaling in the promoting effects of LETX-VI on the synthesis and release of dopamine","authors":"Zhixiang Lei,&nbsp;Haiyan Wang,&nbsp;Yiwen Zhai,&nbsp;Minglu Sun,&nbsp;Si Chen,&nbsp;Panfeng Yin,&nbsp;Xianchun Wang","doi":"10.1007/s12079-023-00783-6","DOIUrl":"10.1007/s12079-023-00783-6","url":null,"abstract":"<div>\u0000 \u0000 <p>Latroeggtoxin-VI (LETX-VI) is an active protein and was previously demonstrated to have effects on the synthesis and release of dopamine. Hererin, the involvement of Ca²⁺ signaling in the effects of LETX-VI on dopamine was systematically investigated, using PC12 cells as a neuron model. LETX-VI was shown to promote dopamine release from PC12 cells both in the presence and absence of extracellular Ca²⁺; however the presence of extracellular Ca²⁺ was favorable for enhancing the promoting effects of LETX-VI on dopamine, because LETX-VI facilitated the influx of extracellular Ca²⁺ through the L-type calcium channels in plasma membrane (PM) to increase cytosolic Ca²⁺ concentration. LETX-VI was able to penetrate the PM of PC12 cells to act on the Ca²⁺ channel proteins IP3Rs and RyRs in the endoplasm reticulum (ER) membrane, opening the Ca²⁺ channels and promoting the release of ER Ca²⁺ to elevate cytosolic Ca²⁺ level. With the help of intracellular Ca²⁺ chelator BAPTA, the elevated cytosolic Ca²⁺ level was proven to play crucial role for the enhanced promoting effects of LETX-VI on dopamine. Taken together, LETX-VI is able to open the Ca²⁺ channels in both PM and ER membrane simultaneously to facilitate extracellular Ca²⁺ influx and ER Ca²⁺ release, and thus increases the cytosolic Ca²⁺ concentration to enhance the promoting effects on the synthesis and release of dopamine.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1309-1321"},"PeriodicalIF":3.6,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10215920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin combined with rapamycin ameliorates podocyte injury in idiopathic membranous nephropathy through the AMPK/mTOR signaling pathway","authors":"Meichen Ma,&nbsp;Yue Pan,&nbsp;Yue Zhang,&nbsp;Mei Yang,&nbsp;Ying Xi,&nbsp;Baoxu Lin,&nbsp;Wudi Hao,&nbsp;Jianhua Liu,&nbsp;Lina Wu,&nbsp;Yong Liu,&nbsp;Xiaosong Qin","doi":"10.1007/s12079-023-00781-8","DOIUrl":"10.1007/s12079-023-00781-8","url":null,"abstract":"<div>\u0000 \u0000 <p>Autophagy activation protects against podocyte injury in idiopathic membranous nephropathy (IMN). The AMPK/mTOR signaling pathway is a vital autophagy regulatory pathway. Metformin promotes autophagy, whereas rapamycin is an autophagy agonist. However, the therapeutic mechanisms of metformin and rapamycin in IMN remain unclear. Thus, we examined the mechanisms of action of metformin and rapamycin in IMN by regulating the AMPK/mTOR autophagy signaling pathway. Female Sprague–Dawley (SD) rats were treated with cationic bovine serum albumin (C-BSA) to establish an IMN model and were randomly divided into IMN model, metformin, rapamycin, and metformin + rapamycin groups. A control group was also established. Metformin and rapamycin were used as treatments. Renal histological changes, urinary protein excretion, the protein expression levels of key AMPK/mTOR signaling pathway proteins, renal tissue cell apoptosis, and autophagy-associated proteins (Beclin 1 and LC3) were examined. In addition, a C5b-9 sublysis model using the MPC-5 mouse podocyte cell line was established to verify the effect of metformin combined with rapamycin on podocytes. Metformin combined with rapamycin improved urinary protein excretion in IMN rats. Metformin combined with rapamycin attenuated the inflammatory response, renal fibrosis, and podocyte foot process fusion. In addition, it improved autophagy in podocytes as demonstrated by the enhanced expression of Beclin-1, p-AMPK/AMPK, LC3-II/I, and autophagosomes in podocytes and decreased p-mTOR/mTOR expression. In conclusion, metformin combined with rapamycin decreased proteinuria, improved renal fibrosis and podocyte autophagy via AMPK/mTOR pathway in IMN rats.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1405-1415"},"PeriodicalIF":3.6,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10222369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin combined with rapamycin ameliorates podocyte injury in idiopathic membranous nephropathy through the AMPK/mTOR signaling pathway.","authors":"Meichen Ma, Yue Pan, Yue Zhang, Mei Yang, Ying Xi, Baoxu Lin, Wudi Hao, Jianhua Liu, Lina Wu, Yong Liu, Xiaosong Qin","doi":"10.2139/ssrn.4257549","DOIUrl":"https://doi.org/10.2139/ssrn.4257549","url":null,"abstract":"Autophagy activation protects against podocyte injury in idiopathic membranous nephropathy (IMN). The AMPK/mTOR signaling pathway is a vital autophagy regulatory pathway. Metformin promotes autophagy, whereas rapamycin is an autophagy agonist. However, the therapeutic mechanisms of metformin and rapamycin in IMN remain unclear. Thus, we examined the mechanisms of action of metformin and rapamycin in IMN by regulating the AMPK/mTOR autophagy signaling pathway. Female Sprague-Dawley (SD) rats were treated with cationic bovine serum albumin (C-BSA) to establish an IMN model and were randomly divided into IMN model, metformin, rapamycin, and metformin + rapamycin groups. A control group was also established. Metformin and rapamycin were used as treatments. Renal histological changes, urinary protein excretion, the protein expression levels of key AMPK/mTOR signaling pathway proteins, renal tissue cell apoptosis, and autophagy-associated proteins (Beclin 1 and LC3) were examined. In addition, a C5b-9 sublysis model using the MPC-5 mouse podocyte cell line was established to verify the effect of metformin combined with rapamycin on podocytes. Metformin combined with rapamycin improved urinary protein excretion in IMN rats. Metformin combined with rapamycin attenuated the inflammatory response, renal fibrosis, and podocyte foot process fusion. In addition, it improved autophagy in podocytes as demonstrated by the enhanced expression of Beclin-1, p-AMPK/AMPK, LC3-II/I, and autophagosomes in podocytes and decreased p-mTOR/mTOR expression. In conclusion, metformin combined with rapamycin decreased proteinuria, improved renal fibrosis and podocyte autophagy via AMPK/mTOR pathway in IMN rats. The metformin and rapamycin decreased proteinuria and inproved renal fibrosis in IMN model rats.","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"1 1","pages":""},"PeriodicalIF":4.1,"publicationDate":"2023-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47747792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression and function of CCN2-derived circRNAs in chondrocytes","authors":"Soma Kato,&nbsp;Kazumi Kawata,&nbsp;Takashi Nishida,&nbsp;Tomomi Mizukawa,&nbsp;Masaharu Takigawa,&nbsp;Seiji Iida,&nbsp;Satoshi Kubota","doi":"10.1007/s12079-023-00782-7","DOIUrl":"10.1007/s12079-023-00782-7","url":null,"abstract":"<div>\u0000 \u0000 <p>Cellular communication network factor 2 (CCN2) molecules promote endochondral ossification and articular cartilage regeneration, and circular RNAs (circRNAs), which arise from various genes and regulate gene expression by adsorbing miRNAs, are known to be synthesized from <i>CCN2</i> in human vascular endothelial cells and other types of cells. However, in chondrocytes, not only the function but also the presence of <i>CCN2</i>-derived circRNA remains completely unknown. In the present study, we investigated the expression and function of <i>CCN2</i>-derived circRNAs in chondrocytes. Amplicons smaller than those from known <i>CCN2</i>-derived circRNAs were observed using RT-PCR analysis that could specifically amplify <i>CCN2</i>-derived circRNAs in human chondrocytic HCS-2/8 cells. The nucleotide sequences of the PCR products indicated novel circRNAs in the HCS-2/8 cells that were different from known <i>CCN2</i>-derived circRNAs. Moreover, the expression of several <i>Ccn2</i>-derived circRNAs in murine chondroblastic ATDC5 cells was confirmed and observed to change alongside chondrocytic differentiation. Next, one of these circRNAs was knocked down in HCS-2/8 cells to investigate the function of the human <i>CCN2</i>-derived circRNA. As a result, <i>CCN2</i>-derived circRNA knockdown significantly reduced the expression of aggrecan mRNA and proteoglycan synthesis. Our data suggest that <i>CCN2</i>-derived circRNAs are expressed in chondrocytes and play a role in chondrogenic differentiation.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1501-1515"},"PeriodicalIF":3.6,"publicationDate":"2023-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10202882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GREM1 signaling in cancer: tumor promotor and suppressor?","authors":"Zhichun Gao,&nbsp;Julia M. Houthuijzen,&nbsp;Peter ten Dijke,&nbsp;Derek P. Brazil","doi":"10.1007/s12079-023-00777-4","DOIUrl":"10.1007/s12079-023-00777-4","url":null,"abstract":"<div>\u0000 \u0000 <p>GREMLIN1 (GREM1) is member of a family of structurally and functionally related secreted cysteine knot proteins, which act to sequester and inhibit the action of multifunctional bone morphogenetic proteins (BMPs). GREM1 binds directly to BMP dimers, thereby preventing BMP-mediated activation of BMP type I and type II receptors. Multiple reports identify the overexpression of GREM1 as a contributing factor in a broad range of cancers. Additionally, the <i>GREM1</i> gene is amplified in a rare autosomal dominant inherited form of colorectal cancer. The inhibitory effects of GREM1 on BMP signaling have been linked to these tumor-promoting effects, including facilitating cancer cell stemness and the activation of cancer-associated fibroblasts. Moreover, GREM1 has been described to bind and signal to vascular endothelial growth factor receptor (VEGFR) and stimulate angiogenesis, as well as epidermal and fibroblast growth factor receptor (EGFR and FGFR) to elicit tumor-promoting effects in breast and prostate cancer, respectively. In contrast, a 2022 report revealed that GREM1 can promote an epithelial state in pancreatic cancers, thereby inhibiting pancreatic tumor growth and metastasis. In this commentary, we will review these disparate findings and attempt to provide clarity around the role of GREM1 signaling in cancer.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1517-1526"},"PeriodicalIF":3.6,"publicationDate":"2023-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10116936","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PKCι induces differential phosphorylation of STAT3 to modify STAT3-related signaling pathways in pancreatic cancer cells","authors":"Junli Wang,&nbsp;Sijia Weng,&nbsp;Yue Zhu,&nbsp;Hongmei Chen,&nbsp;Jueyu Pan,&nbsp;Shuoyu Qiu,&nbsp;Yufeng Liu,&nbsp;Dapeng Wei,&nbsp;Tongbo Zhu","doi":"10.1007/s12079-023-00780-9","DOIUrl":"10.1007/s12079-023-00780-9","url":null,"abstract":"<div>\u0000 \u0000 <p>An increasing number of studies have documented atypical protein kinase C isoform ι (PKCι) as an oncoprotein playing multifaceted roles in pancreatic carcinogenesis, including sustaining the transformed growth, prohibiting apoptosis, strengthening invasiveness, facilitating autophagy, as well as promoting the immunosuppressive tumor microenvironment of pancreatic tumors. In this study, we present novel evidence that PKCι overexpression increases STAT3 phosphorylation at the Y705 residue while decreasing STAT3 phosphorylation at the S727 residue in pancreatic cancer cells. We further demonstrate that STAT3 phosphorylation at Y705 and S727 residues is mutually antagonistic, and that STAT3 Y705 phosphorylation is positively related to the transcriptional activity of STAT3 in pancreatic cancer cells. Furthermore, we discover that PKCι inhibition attenuates STAT3 transcriptional activity via Y705 dephosphorylation, which appears to be resulted from enhanced phosphorylation of S727 in pancreatic cancer cells. Finally, we investigate and prove that by modulating the STAT3 activity, the PKCι inhibitor can synergistically enhance the antitumor effects of pharmacological STAT3 inhibitors or reverse the anti-apoptotic side effects incited by the MEK inhibitor, thereby posing as a prospective sensitizer in the treatment of pancreatic cancer cells.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1417-1433"},"PeriodicalIF":3.6,"publicationDate":"2023-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713918/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10001137","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Role of EGFR and FASN in breast cancer progression","authors":"Suchi Chaturvedi,&nbsp;Mainak Biswas,&nbsp;Sushabhan Sadhukhan,&nbsp;Avinash Sonawane","doi":"10.1007/s12079-023-00771-w","DOIUrl":"10.1007/s12079-023-00771-w","url":null,"abstract":"<div>\u0000 \u0000 <p>Breast cancer (BC) emerged as one of the life-threatening diseases among females. Despite notable improvements made in cancer detection and treatment worldwide, according to GLOBACAN 2020, BC is the fifth leading cancer, with an estimated 1 in 6 cancer deaths, in a majority of countries. However, the exact cause that leads to BC progression still needs to be determined. Here, we reviewed the role of two novel biomarkers responsible for 50–70% of BC progression. The first one is epidermal growth factor receptor (EGFR) which belongs to the ErbB tyrosine kinases family, signalling pathways associated with it play a significant role in regulating cell proliferation and division. Another one is fatty acid synthase (FASN), a key enzyme responsible for the de novo lipid synthesis required for cancer cell development. This review presents a rationale for the EGFR-mediated pathways, their interaction with FASN, communion of these two biomarkers with BC, and improvements to overcome drug resistance caused by them.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1249-1282"},"PeriodicalIF":3.6,"publicationDate":"2023-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9866677","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of ZMYND19 as a novel biomarker of colorectal cancer: RNA-sequencing and machine learning analysis","authors":"Ghazaleh Khalili-Tanha,&nbsp;Reza Mohit,&nbsp;Alireza Asadnia,&nbsp;Majid Khazaei,&nbsp;Mohammad Dashtiahangar,&nbsp;Mina Maftooh,&nbsp;Mohammadreza Nassiri,&nbsp;Seyed Mahdi Hassanian,&nbsp;Majid Ghayour-Mobarhan,&nbsp;Mohammad Ali Kiani,&nbsp;Gordon A. Ferns,&nbsp;Jyotsna Batra,&nbsp;Elham Nazari,&nbsp;Amir Avan","doi":"10.1007/s12079-023-00779-2","DOIUrl":"10.1007/s12079-023-00779-2","url":null,"abstract":"<div>\u0000 \u0000 <p>Colorectal cancer (CRC) is the third most common cause of cancer-related deaths. The five-year relative survival rate for CRC is estimated to be approximately 90% for patients diagnosed with early stages and 14% for those diagnosed at an advanced stages of disease, respectively. Hence, the development of accurate prognostic markers is required. Bioinformatics enables the identification of dysregulated pathways and novel biomarkers. RNA expression profiling was performed in CRC patients from the TCGA database using a Machine Learning approach to identify differential expression genes (DEGs). Survival curves were assessed using Kaplan–Meier analysis to identify prognostic biomarkers. Furthermore, the molecular pathways, protein–protein interaction, the co-expression of DEGs, and the correlation between DEGs and clinical data have been evaluated. The diagnostic markers were then determined based on machine learning analysis. The results indicated that key upregulated genes are associated with the RNA processing and heterocycle metabolic process, including C10orf2, NOP2, DKC1, BYSL, RRP12, PUS7, MTHFD1L, and PPAT. Furthermore, the survival analysis identified NOP58, OSBPL3, DNAJC2, and ZMYND19 as prognostic markers. The combineROC curve analysis indicated that the combination of C10orf2 -PPAT- ZMYND19 can be considered as diagnostic markers with sensitivity, specificity, and AUC values of 0.98, 1.00, and 0.99, respectively. Eventually, ZMYND19 gene was validated in CRC patients. In conclusion, novel biomarkers of CRC have been identified that may be a promising strategy for early diagnosis, potential treatment, and better prognosis.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1469-1485"},"PeriodicalIF":3.6,"publicationDate":"2023-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713961/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9764247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"High expression of GPR50 promotes the proliferation, migration and autophagy of hepatocellular carcinoma cells in vitro","authors":"Weiming Zhao,&nbsp;Lingling Xi,&nbsp;Guoying Yu,&nbsp;Gaiping Wang,&nbsp;Cuifang Chang","doi":"10.1007/s12079-023-00772-9","DOIUrl":"10.1007/s12079-023-00772-9","url":null,"abstract":"<div>\u0000 \u0000 <p>G protein-coupled receptors (GPCRs) play important roles in tumorigenesis and the development of hepatocellular carcinoma (HCC). GPR50 is an orphan GPCR. Previous studies have indicated that GPR50 could protect against breast cancer development and decrease tumor growth in a xenograft mouse model. However, its role in HCC remains indistinct. To detect the role and the regulation mechanism of GPR50 in HCC, GPR50 expression was analyzed in HCC patients (gene expression omnibus database (GEO) (GSE45436)) and detected in HCC cell line CBRH-7919, and the results showed that GPR50 was significantly up-regulated in HCC patients and CBRH-7919 cell line compared to the corresponding normal control. <i>Gpr50</i> cDNA was transfected into HCC cell line CBRH-7919, and we found that <i>Gpr50</i> promoted the proliferation, migration, and autophagy of CBRH-7919. The regulation mechanism of GPR50 in HCC was detected by isobaric tags for relative and absolute quantification (iTRAQ) analysis, and we found that GPR50 promoted HCC was closely related to CCT6A and PGK1. Taken together, GPR50 may promote HCC progression via CCT6A-induced proliferation and PGK1-induced migration and autophagy, and GPR50 could be an important target for HCC.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1435-1447"},"PeriodicalIF":3.6,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713896/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9696419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The advance of CCN3 in fibrosis","authors":"Hui Yin,&nbsp;Na Liu,&nbsp;Xianming Zhou,&nbsp;Jie Chen,&nbsp;Lihua Duan","doi":"10.1007/s12079-023-00778-3","DOIUrl":"10.1007/s12079-023-00778-3","url":null,"abstract":"<div>\u0000 \u0000 <p>The extracellular matrix (ECM) is comprised of various extracellular macromolecules, including collagen, enzymes, and glycoproteins, which offer structural and biochemical support to neighboring cells. After tissue injury, extracellular matrix proteins deposit in the damaged tissue to promote tissue healing. However, an imbalance between ECM production and degradation can result in excessive deposition, leading to fibrosis and subsequent organ dysfunction. Acting as a regulatory protein within the extracellular matrix, CCN3 plays a crucial role in numerous biological processes, such as cell proliferation, angiogenesis, tumorigenesis, and wound healing. Many studies have demonstrated that CCN3 can reduce the production of ECM in tissues through diverse mechanisms thereby exerting an inhibitory effect on fibrosis. Consequently, CCN3 emerges as a promising therapeutic target for ameliorating fibrosis.</p>\u0000 </div>","PeriodicalId":15226,"journal":{"name":"Journal of Cell Communication and Signaling","volume":"17 4","pages":"1219-1227"},"PeriodicalIF":3.6,"publicationDate":"2023-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10713972/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9696423","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}