Journal of Cellular and Molecular Medicine最新文献

{"title":"Immunosuppressive SOX9-AS1 Resists Triple-Negative Breast Cancer Senescence Via Regulating Wnt Signalling Pathway.","authors":"Xuan Ye, Yi Cen, Quan Li, Yuan-Ping Zhang, Qian Li, Jie Li","doi":"10.1111/jcmm.70208","DOIUrl":"10.1111/jcmm.70208","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) are involved in the regulation of triple-negative breast cancer (TNBC) senescence, while pro-carcinogenic lncRNAs resist senescence onset leading to the failure of therapy-induced senescence (TIS) strategy, urgently identifying the key senescence-related lncRNAs (SRlncRNAs). We mined seven SRlncRNAs (SOX9-AS1, LINC01152, AC005152.3, RP11-161 M6.2, RP5-968 J1.1, RP11-351 J23.1 and RP11-666A20.3) by bioinformatics, of which SOX9-AS1 was reported to be pro-carcinogenic. In vitro experiments revealed the highest expression of SOX9-AS1 in MDA-MD-231 cells. SOX9-AS1 knockdown inhibited cell growth (proliferation, cycle and apoptosis) and malignant phenotypes (migration and invasion), while SOX9-AS1 overexpression rescued these effects. Additionally, SOX9-AS1 knockdown facilitated tamoxifen-induced cellular senescence and the transcription of senescence-associated secretory phenotype (SASP) factors (IL-1α, IL-1β, IL-6 and IL-8) mechanistically by resisting senescence-induced Wnt signal (GSK-3β/β-catenin) activation. Immune infiltration analysis revealed that low SOX9-AS1 expression was accompanied by a high infiltration of naïve B cells, CD8⁺ T cells and γδ T cells. In conclusion, SOX9-AS1 resists TNBC senescence via regulating the Wnt signalling pathway and inhibits immune infiltration. Targeted inhibition of SOX9-AS1 enhances SASP and thus mobilises immune infiltration to adjunct TIS strategy.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"28 22","pages":"e70208"},"PeriodicalIF":5.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70208","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644326","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the Immune Landscape of ccRCC: Prognostic Signatures and Therapeutic Implications.","authors":"Minjie Pan, Xinchi Xu, Dong Zhang, Wei Cao","doi":"10.1111/jcmm.70212","DOIUrl":"10.1111/jcmm.70212","url":null,"abstract":"<p><p>The tumour immunological microenvironment is involved in the development of clear cell renal cell carcinoma (ccRCC). Nevertheless, the role of the immunological microenvironment in ccRCC has not been thoroughly investigated. In this study, we combined six ccRCC cohorts into a large cohort and quantified the expression matrix into 53 immunological terms using the ssGSEA algorithm. Five immune terms related to prognosis were screened through 1000 iterations of L1-penalised (lasso) estimation and Cox regression analysis for immune-related risk score (IRS) calculation. The IRS showed satisfactory prognosis prediction efficacy in ccRCC. We then compared the clinical and genomic characteristics of two IRS subgroups. Patients with low IRS showed a high level of tumour mutational burden (TMB) and a low level of copy number variation (CNV), indicating that low IRS group patients have a higher probability of responding to immunotherapy. We employed TIDE and subclass mapping analyses to corroborate our results, and the findings demonstrated that patients with a low IRS had a significantly greater percentage of immunotherapy response. According to the Genomics of Drug Sensitivity in Cancer (GDSC), patients with a high IRS had a decreased IC50 for sunitinib, which is the first-line treatment for ccRCC patients. As a result, the immune characteristics of the microenvironment of ccRCC tumours have been explored, and a signature has been constructed. Analysis demonstrated that our signature could effectively predict prognosis and immunotherapy response rate.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"28 22","pages":"e70212"},"PeriodicalIF":5.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11573483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Associations of genetic variation and mRNA expression of PDGF/PDGFRB pathway genes with coronary artery disease in the Chinese population.","authors":"Pengfei Wei, Hankun Xie, Junxiang Sun, Qian Zhuang, Jichao Xie, Yunjie Yin, Fangyuan Liu, Wen Li, Changying Chen, Feifan Wang, Xu Han, Liang Xu, Xianghai Zhao, Yanchun Chen, Song Yang, Chong Shen","doi":"10.1111/jcmm.70193","DOIUrl":"https://doi.org/10.1111/jcmm.70193","url":null,"abstract":"<p><p>Platelet-derived growth factors (PDGFs) and receptors (PDGFR) play a key role in the process of coronary atherosclerosis. We aimed to investigate the association of genetic variations and mRNA expressions of PDGF/PDGFRB pathway genes with coronary artery disease (CAD). In this case-control study (3139 CAD vs. 3270 controls), 13 single nucleotide polymorphisms (SNPs) at five pathway genes were genotyped and combined to construct a weighted genetic risk score (wGRS). Three hundred and six pairs of cases and controls were selected for mRNA quantification. Restricted cubic spline (RCS) analyses were conducted for the dose-response relationship between wGRS, mRNAs and CAD. Area under the curve (AUC) was estimated to evaluate the discrimination of wGRS, mRNAs, and traditional risk factors (TRF) for CAD. The wGRS exhibited a positive linear relationship with CAD (p for linearity <0.001), and the medium and high wGRS had 37% and 50% increased risk of CAD compared to the low wGRS group (p = 1.5 × 10^-4; p = 5.7 × 10^-5). mRNA expression levels of five genes in peripheral blood leukocytes were all lower among patients at admission than controls (p < 0.001). The PDGF/PDGFRB mRNA expressions had significant non-linear correlations with AMI, with \"U\"-shaped trend for PDGFA, PDGFB and \"L\"-shaped trend for PDGFC, PDGFD and PDGFRB. Adding wGRS and mRNAs to the TRF model significantly improved the discrimination for CAD with an AUC of 0.921 (95% CI, 0.898-0.943). Genetic variations in the PDGF/PDGFRB pathway contribute to CAD susceptibility with a significantly joint effect. The down-regulated PDGF/PDGFRB mRNAs in peripheral leukocytes have the potential as blood-based biomarkers for CAD with high discriminative value.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"28 22","pages":"e70193"},"PeriodicalIF":5.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142681872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nodularin-R Synergistically Enhances Abiraterone Against Castrate- Resistant Prostate Cancer via PPP1CA Inhibition.","authors":"Yiqiao Huang, Yi Cen, Hualing Wu, Guohao Zeng, Zhengming Su, Zhiming Zhang, Shourui Feng, Xianhan Jiang, Anyang Wei","doi":"10.1111/jcmm.70210","DOIUrl":"10.1111/jcmm.70210","url":null,"abstract":"<p><p>Clinically, most prostate cancer (PCa) patients inevitably progress to castration-resistant prostate cancer (CRPC) with poor prognosis after androgen deprivation therapy (ADT), including abiraterone, the drug of choice for ADT. Therefore, it is necessary to explore the resistance mechanism of abiraterone in depth. Genome-wide CRISPR/Cas9 knockout technology was used to screen CRPC cell line 22Rv1 for abiraterone-resistant genes. Combined with bioinformatics, a key gene with high expression and poor prognosis in CRPC patients was screened. Then, the effects of target gene on abiraterone-resistant 22Rv1 cell function were explored by silencing and overexpression. Further, a natural product with potential targeting effect was identified and validated by molecular docking and protein expression. Molecular dynamics simulations revealed potential mechanism for the natural product affecting target protein expression. Finally, the combined anti-CRPC effects of the natural product and abiraterone were validated by cellular and in vivo experiments. Five common resistance genes (KCNJ3, COL2A1, PPP1CA, MDH2 and EXOSC5) were identified successfully, among which high PPP1CA expression had the worst prognosis for disease-free survival. Moreover, PPP1CA was highly expressed in abiraterone-resistant 22Rv1 cells. Silencing PPP1CA increased cell sensitivity to abiraterone while promoting apoptosis and inhibiting clone formation. Overexpressing PPP1CA exerted the opposite effects. Molecular docking revealed the binding mode of the natural product nodularin-R to PPP1CA with a dose-dependent manner for inhibition. Mechanistically, nodularin-R attenuates the interaction between PPP1CA and USP11 (deubiquitinating enzyme), potentially promoting PPP1CA degradation. Additionally, combination of 2.72 μM nodularin-R and 54.5 μM abiraterone synergistically inhibited the resistant 22Rv1 cell function. In vivo experiments also revealed that combination therapy significantly inhibited tumour growth and reduced inducible expression of PPP1CA. PPP1CA is a key driver for abiraterone resistance, and nodularin-R enhances the anti-CRPC effects of abiraterone by inhibiting PPP1CA.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"28 22","pages":"e70210"},"PeriodicalIF":5.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.70210","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142644328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperbaric oxygen therapy suppresses hypoxia and reoxygenation injury to retinal pigment epithelial cells through activating peroxisome proliferator activator receptor-alpha signalling","authors":"Tzong-Bor Sun,&nbsp;Kuo-Feng Huang,&nbsp;Ko-Chi Niu,&nbsp;Cheng-Hsien Lin,&nbsp;Wen-Pin Liu,&nbsp;Chao-Hung Yeh,&nbsp;Shu-Chun Kuo,&nbsp;Ching-Ping Chang","doi":"10.1111/jcmm.17963","DOIUrl":"10.1111/jcmm.17963","url":null,"abstract":"<p>Retinal ischemia followed by reperfusion (IR) is a common cause of many ocular disorders, such as age-related macular degeneration (AMD), which leads to blindness in the elderly population, and proper therapies remain unavailable. Retinal pigment epithelial (RPE) cell death is a hallmark of AMD. Hyperbaric oxygen (HBO) therapy can improve IR tissue survival by inducing ischemic preconditioning responses. We conducted an in vitro study to examine the effects of HBO preconditioning on oxygen–glucose deprivation (OGD)-induced IR-injured RPE cells. RPE cells were treated with HBO (100% O₂ at 3 atmospheres absolute for 90 min) once a day for three consecutive days before retinal IR onset. Compared with normal cells, the IR-injured RPE cells had lower cell viability, lower peroxisome proliferator activator receptor-alpha (PPAR-α) expression, more severe oxidation status, higher blood-retinal barrier disruption and more elevated apoptosis and autophagy rates. HBO preconditioning increased PPAR-α expression, improved cell viability, decreased oxidative stress, blood-retinal barrier disruption and cellular apoptosis and autophagy. A specific PPAR-α antagonist, GW6471, antagonized all the protective effects of HBO preconditioning in IR-injured RPE cells. Combining these observations, HBO therapy can reverse OGD-induced RPE cell injury by activating PPAR-α signalling.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"27 20","pages":"3189-3201"},"PeriodicalIF":5.3,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.17963","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41139598","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Transcriptome analysis of six tissues obtained post-mortem from sepsis patients","authors":"Fabiano Pinheiro da Silva,&nbsp;André Nicolau Aquime Gonçalves,&nbsp;Amaro Nunes Duarte-Neto,&nbsp;Thomaz Lüscher Dias,&nbsp;Hermes Vieira Barbeiro,&nbsp;Cristiane Naffah Souza Breda,&nbsp;Leandro Carvalho Dantas Breda,&nbsp;Niels Olsen Saraiva Câmara,&nbsp;Helder I. Nakaya","doi":"10.1111/jcmm.17938","DOIUrl":"10.1111/jcmm.17938","url":null,"abstract":"<p>Septic shock is a life-threatening clinical condition characterized by a robust immune inflammatory response to disseminated infection. Little is known about its impact on the transcriptome of distinct human tissues. To address this, we performed RNA sequencing of samples from the prefrontal cortex, hippocampus, heart, lung, kidney and colon of seven individuals who succumbed to sepsis and seven uninfected controls. We identified that the lungs and colon were the most affected organs. While gene activation dominated, strong inhibitory signals were also detected, particularly in the lungs. We found that septic shock is an extremely heterogeneous disease, not only when different individuals are investigated, but also when comparing different tissues of the same patient. However, several pathways, such as respiratory electron transport and other metabolic functions, revealed distinctive alterations, providing evidence that tissue specificity is a hallmark of sepsis. Strikingly, we found evident signals of accelerated ageing in our sepsis population.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"27 20","pages":"3157-3167"},"PeriodicalIF":5.3,"publicationDate":"2023-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.17938","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41132144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Selenium in combination with a tomato lipid extract as a therapy for benign prostatic hyperplasia and its alterations in rats with induced BPH","authors":"David Julian Arias-Chávez,&nbsp;Patrick Mailloux-Salinas,&nbsp;Jessica Ledesma Aparicio,&nbsp;Elihu Campos-Pérez,&nbsp;Omar Noel Medina-Campos,&nbsp;José Pedraza-Chaverri,&nbsp;Guadalupe Bravo","doi":"10.1111/jcmm.17903","DOIUrl":"10.1111/jcmm.17903","url":null,"abstract":"<p>Benign prostatic hyperplasia (BPH) is the most common adenoma in old men. Tomatoes are a rich source of bioactive compounds that, as well as selenium (Se), possess antioxidant and antiproliferative activity. The aim was to evaluate the therapeutic effect of Se in combination with a tomato extract in aged rats with BPH. Aged male Wistar rats were divided in the following groups (<i>n</i> = 10 rats/group): Control (C), BPH, BPH + Finasteride (BPH + F), BPH + Tomato Lipidic Extract (BPH + E), BPH + Selenium (BPH + S) and BPH plus E plus S (BPH + E + S). After 4 weeks of treatment, prostate weight, diuresis, antioxidants enzymes, prooxidants and inflammatory markers, growth factors and androgens were determined. BPH + E + S reduced prostate weight by 59.29% and inhibited growth by 99.35% compared to BPH + F which only decreased weight and inhibited growth by 15.31% and 57.54%, respectively. Prooxidant markers were higher with BPH + F (49.4% higher vs. BPH), but BPH + E + S decreased these markers (94.27% vs. BPH) and increased antioxidant activity. Finally, diuresis was higher with the BPH + E + S combination and markers of inflammation and growth factors were significantly lower with respect to BPH + F. Our findings provide a beneficial and protective therapeutic option of E + S directed against androgens, oxidative stress and inflammation that regulates cell proliferation in the prostate gland.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"27 20","pages":"3147-3156"},"PeriodicalIF":5.3,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.17903","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41140470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antimalarial drug discovery against malaria parasites through haplopine modification: An advanced computational approach","authors":"Shopnil Akash,&nbsp;Guendouzi Abdelkrim,&nbsp;Imren Bayil,&nbsp;Md. Eram Hosen,&nbsp;Nobendu Mukerjee,&nbsp;Abdullah F. Shater,&nbsp;Fayez M. Saleh,&nbsp;Ghadeer M. Albadrani,&nbsp;Muath Q. Al-Ghadi,&nbsp;Mohamed M. Abdel-Daim,&nbsp;Tuğba Taşkin Tok","doi":"10.1111/jcmm.17940","DOIUrl":"10.1111/jcmm.17940","url":null,"abstract":"<p>The widespread emergence of antimalarial drug resistance has created a major threat to public health. Malaria is a life-threatening infectious disease caused by <i>Plasmodium</i> spp., which includes Apicoplast DNA polymerase and <i>Plasmodium falciparum</i> cysteine protease falcipain-2. These components play a critical role in their life cycle and metabolic pathway, and are involved in the breakdown of erythrocyte hemoglobin in the host, making them promising targets for anti-malarial drug design. Our current study has been designed to explore the potential inhibitors from haplopine derivatives against these two targets using an in silico approach. A total of nine haplopine derivatives were used to perform molecular docking, and the results revealed that Ligands 03 and 05 showed strong binding affinity compared to the control compound atovaquone. Furthermore, these ligand-protein complexes underwent molecular dynamics simulations, and the results demonstrated that the complexes maintained strong stability in terms of RMSD (root mean square deviation), RMSF (root mean square fluctuation), and Rg (radius of gyration) over a 100 ns simulation period. Additionally, PCA (principal component analysis) analysis and the dynamic cross-correlation matrix showed positive outcomes for the protein-ligand complexes. Moreover, the compounds exhibited no violations of the Lipinski rule, and ADMET (absorption, distribution, metabolism, excretion, and toxicity) predictions yielded positive results without indicating any toxicity. Finally, density functional theory (DFT) and molecular electrostatic potential calculations were conducted, revealing that the mentioned derivatives exhibited better stability and outstanding performance. Overall, this computational approach suggests that these haplopine derivatives could serve as a potential source for developing new, effective antimalarial drugs to combat malaria. However, further in vitro or in vivo studies might be conducted to determine their actual effectiveness.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"27 20","pages":"3168-3188"},"PeriodicalIF":5.3,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.17940","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41126537","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to Chronic stress inhibits testosterone synthesis in Leydig cells through mitochondrial damage via Atp5a1","authors":"","doi":"10.1111/jcmm.17829","DOIUrl":"10.1111/jcmm.17829","url":null,"abstract":"<p>In Xiaofan Xiong et al,<span>¹</span> the spots number of ‘224’ and ‘246’ in Figure 3B mismatch with the spots of ‘234’ and ‘236’ in Figure 3C due to technical error. In addition, the spots name of ‘246’ in Table 1 mismatch with the spots of ‘236’ in Figure 3C. The correct Figure 3 and Table 1 are shown below. The authors confirmed that all results and conclusions of this article remain unchanged.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"27 20","pages":"3213-3214"},"PeriodicalIF":5.3,"publicationDate":"2023-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.17829","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10363181","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to Down-regulated lncRNA SLC25A5-AS1 facilitates cell growth and inhibits apoptosis via miR-19a-3p/PTEN/PI3K/AKT signalling pathway in gastric cancer","authors":"","doi":"10.1111/jcmm.17830","DOIUrl":"10.1111/jcmm.17830","url":null,"abstract":"<p>In Xiwen Li et al.,<span>¹</span> the colony formation analyses for BGC-823 (vector) and SGC-7901 of Figure 3B are incorrect. In addition, the labels for BGC-823 and SGC-7901 are reverse in Figure 3E. The correct figures are shown below. The authors confirm that all results and conclusions of this article remain unchanged.</p>","PeriodicalId":15215,"journal":{"name":"Journal of Cellular and Molecular Medicine","volume":"27 20","pages":"3215-3216"},"PeriodicalIF":5.3,"publicationDate":"2023-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.17830","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10314667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}