Aging最新文献

{"title":"Association between Epstein-Barr virus serological reactivation and psychological distress: a cross-sectional study of Japanese community-dwelling older adults.","authors":"Hirotomo Yamanashi,&nbsp;Shogo Akabame,&nbsp;Jun Miyata,&nbsp;Yukiko Honda,&nbsp;Fumiaki Nonaka,&nbsp;Yuji Shimizu,&nbsp;Seiko Nakamichi,&nbsp;Shin-Ya Kawashiri,&nbsp;Mami Tamai,&nbsp;Kazuhiko Arima,&nbsp;Atsushi Kawakami,&nbsp;Kiyoshi Aoyagi,&nbsp;Takahiro Maeda","doi":"10.18632/aging.204345","DOIUrl":"https://doi.org/10.18632/aging.204345","url":null,"abstract":"<p><p>Reactivation of Epstein-Barr virus (EBV) is associated with the etiopathogenesis of a broad spectrum of diseases. This study aimed to investigate the association between psychological distress and EBV serological reactivation among community-dwelling older people and assess the role of sex differences in this association. This population-based cross-sectional survey was conducted among individuals who underwent annual health checkups (N = 2,821; median age 72.4 years). EBV serological reactivation was defined as elevation of EBV early antigen immunoglobulin G titers, and psychological distress was defined as Kessler 6 scores ≥5. Multivariable logistic regression analysis was performed to calculate odds ratios (OR) and 95% confidence intervals (CI) for EBV serological reactivation and psychological distress. EBV serological reactivation and psychological distress were detected in 16.4% and 8.7% of participants, respectively. Women accounted for 71% (328/463) of those with EBV serological reactivation. Multivariable logistic regression analysis showed psychological distress was not significantly associated with EBV serological reactivation among all participants (OR 1.31, 95% CI: 0.95, 1.82; P = 0.102). A sex-stratified multivariable analysis showed a positive association among women (OR 1.45, 95% CI: 1.01, 2.08; P = 0.043), but no association among men. EBV serological reactivation was independently associated with psychological distress in community-dwelling older women. The sex difference in our results warrants further investigation to clarify the physiological mechanisms underlying the association.</p>","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8258-8269"},"PeriodicalIF":5.2,"publicationDate":"2022-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9648801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40667751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Network analysis for the identification of hub genes and related molecules as potential biomarkers associated with the differentiation of bone marrow-derived stem cells into hepatocytes.","authors":"Ying-Hao Han,&nbsp;Xin-Mei He,&nbsp;Seung-Jae Lee,&nbsp;Ying-Ying Mao,&nbsp;Xuan-Chen Liu,&nbsp;Hu-Nan Sun,&nbsp;Mei-Hua Jin,&nbsp;Taeho Kwon","doi":"10.18632/aging.204344","DOIUrl":"https://doi.org/10.18632/aging.204344","url":null,"abstract":"<p><p>The incidence of liver diseases has been increasing steadily. However, it has some shortcomings, such as high cost and organ donor scarcity. The application of stem cell research has brought new ideas for the treatment of liver diseases. Therefore, it is particularly important to clarify the molecular and regulatory mechanisms of differentiation of bone marrow-derived stem cells (BMSCs) into liver cells. Herein, we screened differentially expressed genes between hepatocytes and untreated BMSCs to identify the genes responsible for the differentiation of BMSCs into hepatocytes. GSE30419 gene microarray data of BMSCs and GSE72088 gene microarray data of primary hepatocytes were obtained from the Gene Expression Omnibus database. Transcriptome Analysis Console software showed that 1896 genes were upregulated and 2506 were downregulated in hepatocytes as compared with BMSCs. Hub genes were analyzed using the STRING and Cytoscape v 3.8.2, revealing that twenty-four hub genes, play a pivotal role in the differentiation of BMSCs into hepatocytes. The expression of the hub genes in the BMSCs and hepatocytes was verified by reverse transcription-quantitative PCR (RT-qPCR). Next, the target miRNAs of hub genes were predicted, and then the lncRNAs regulating miRNAs was discovered, thus forming the lncRNA-miRNA-mRNA interaction chain. The results indicate that the lncRNA-miRNA-mRNA interaction chain may play an important role in the differentiation of BMSCs into hepatocytes, which provides a new therapeutic target for liver disease treatment.</p>","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8243-8257"},"PeriodicalIF":5.2,"publicationDate":"2022-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9648814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40667752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renoprotective effect of Tanshinone IIA against kidney injury induced by ischemia-reperfusion in obese rats.","authors":"He Tai,&nbsp;Xiao-Zheng Cui,&nbsp;Jia He,&nbsp;Zhi-Ming Lan,&nbsp;Shun-Min Li,&nbsp;Ling-Bing Li,&nbsp;Si-Cheng Yao,&nbsp;Xiao-Lin Jiang,&nbsp;Xian-Sheng Meng,&nbsp;Jin-Song Kuang","doi":"10.18632/aging.204304","DOIUrl":"https://doi.org/10.18632/aging.204304","url":null,"abstract":"<p><strong>Objective: </strong>Obesity enhances the frequency and severity of acute kidney injury (AKI) induced by renal ischemia-reperfusion (IR). Tanshinone IIA (TIIA) pre-treatment was used to alleviate renal injury induced by renal IR, and whether TIIA can attenuate renal cell apoptosis via modulating mitochondrial function through PI3K/Akt/Bad pathway in obese rats was examined.</p><p><strong>Methods: </strong>Male rates were fed a high-fat diet for 8 weeks to generate obesity, followed by 30 min of kidney ischemia and 24 h reperfusion induced AKI. The male obese rates were given TIIA (5 mg/kg.d, 10 mg/kg.d, and 20 mg/kg.d) for 2 weeks before renal IR.</p><p><strong>Results: </strong>TIIA alleviated the pathohistological injury and apoptosis induced by IR. In addition, TIIA improved renal function, inflammatory factor, and balance of oxidation and antioxidation in obese rats after renal IR. At the same time, TIIA can inhibit cell apoptosis by improving mitochondrial function through the PI3K/Akt/Bad pathway. Mitochondrial dysfunction was supported by decreasing intracellular ATP, respiration controlling rate (RCR), mitochondrial membrane potential (MMP), and mitochondrial respiratory chain complex enzymes, and by increasing ROS, the opening of mitochondrial permeability transition pore (mPTP), and the mtDNA damage. The injury to mitochondrial dynamic function was assessed by decreasing Drp1, and increasing Mfn1/2; and the injury of mitochondrial biogenesis was assessed by decreasing PGC-1, Nrf1, and TFam.</p><p><strong>Conclusions: </strong>Renal mitochondrial dysfunction occurs along with renal IR and can induce renal cell apoptosis. Obesity can aggravate apoptosis. TIIA can attenuate renal cell apoptosis via modulating mitochondrial function through PI3K/Akt/Bad pathway in obese rats.</p>","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8302-8320"},"PeriodicalIF":5.2,"publicationDate":"2022-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9648803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40667754","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identify miRNA-mRNA regulation pairs to explore potential pathogenesis of lung adenocarcinoma.","authors":"Xingchen Fan,&nbsp;Xuan Zou,&nbsp;Cheng Liu,&nbsp;Shuang Peng,&nbsp;Shiyu Zhang,&nbsp;Xin Zhou,&nbsp;Jun Zhu,&nbsp;Wei Zhu","doi":"10.18632/aging.204341","DOIUrl":"https://doi.org/10.18632/aging.204341","url":null,"abstract":"<p><strong>Purpose: </strong>MicroRNA (miRNA) function via base-pairing with complementary sequences within mRNA molecules. This study aims to identify critical miRNA-mRNA regulation pairs contributing to lung adenocarcinoma (LUAD) pathogenesis.</p><p><strong>Patients and methods: </strong>MiRNA and mRNA microarray and RNA-sequencing datasets were downloaded from gene expression omnibus (GEO) and the cancer genome atlas (TCGA) databases. Differential miRNAs (DE-miRNAs) and mRNAs (DE-mRNAs) were screened by the GEO2R tool and R packages. DAVID, DIANA, and Hiplot tools were used to perform gene enrichment analysis. The pairs of miRNA-mRNA were screened from the experimentally validated miRNA-target interactions databases (miRTarBase and TarBase). External validation was carried out in 30 pairs of LUAD tissues by quantitative reverse transcription and polymerase chain reaction (qRT-PCR). The diagnostic value of the miRNA-mRNA regulation pairs was evaluated by receiver operating characteristic curve (ROC) and decision curve analysis (DCA). Biological function assay was were also performed to confirm the function of miRNA-mRNA axis in LUAD progression. The study also performed the clinical, survival and tumor-associated phenotypic analysis of miRNA-mRNA pairs.</p><p><strong>Results: </strong>A total of 7 miRNA and 13 mRNA expression datasets from GEO were analyzed, and 11 DE-miRNAs (5 down-regulated and 6 up-regulated in LUAD tissues) and 128 DE-mRNAs (30 up-regulated and 98 down-regulated in LUAD tissues) were identified. The pairs of miR-1-3p(down) and CENPF(up) and miR-126-5p(down) and UGT8(up) were verified in the external validation cohort (30 LUAD vs. 30 NC) using qRT-PCR. Areas under the ROC curve of the two miRNA-mRNA regulation pairs panel were 0.973 in TCGA-LUAD and 0.771 in the external validation. The DCA also showed that the miRNA-mRNA regulation pairs had an excellent diagnostic performance distinguishing LUAD from normal controls. The expression of the regulation pairs is different in different ages, TNM stages, and gender. The overexpression of miR-1-3p and miR-126-5p significantly inhibited the proliferation and migration of LUAD cells. Correlation analysis showed that CENPF correlated with prognosis and tumor immunity.</p><p><strong>Conclusions: </strong>The research identified potential miRNA-mRNA regulation pairs, providing a new idea for exploring the genesis and development of LUAD.</p>","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8357-8373"},"PeriodicalIF":5.2,"publicationDate":"2022-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9648793/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40343163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Parthenolide targets NF-κB (P50) to inhibit HIF-1α-mediated metabolic reprogramming of HCC.","authors":"Xiaorong Liu,&nbsp;Zhaofeng Gao,&nbsp;Xiaoguang Wang,&nbsp;Yiyu Shen","doi":"10.18632/aging.204339","DOIUrl":"https://doi.org/10.18632/aging.204339","url":null,"abstract":"<p><p>We focus on investigating the role of Parthenolide (Par), a small sesquiterpenoid molecule, in hepatocellular carcinoma (HCC) and its effective target.Highly-metastatic HCC cells, MHCC97-H, were divided into the DMSO and the Par groups, of which the Par group was intervened at 5 and 10 mg/L doses. Cell viability was assessed by CCK-8 assay. Transwell chamber assay was performed to examine the metastatic and invasive abilities, while plate clone formation assay was conducted to detect the clone formation ability. For analysis of glucose uptake, glycolytic ability and lactate level, the glycolysis assay was employed. Brdu staining was performed to evaluate the cell proliferative potential. The P50 and HIF-1α levels were measured by immunofluorescence, while the expressions of p-P50 and HIF-1α were determined by Western-Blot. Small molecule-protein docking and Pull-down experiments were conducted to validate the Par-P50 binding model. After establishing the tumor-bearing mouse model, Par was administered by gavage to measure the tissue levels of P50 and HIF-1α, followed by plotting of tumor growth curves.Par could inhibit the metastatic, invasive and clone formation abilities of MHCC97-H cells, reduce the cell proliferative potential, and suppress the glycolysis, as manifested by down-regulated level of lactate and reduced oxygen consumption. Meanwhile, Par inhibited the HIF-1α expression. We found that after silencing P50, the HIF-1α was down-regulated, the glycolytic ability decreased drastically, and the cellular metastatic and invasive abilities were suppressed. After P50 knockout, the effect of Par intervention on the MHCC97-H cells was reduced. In HCC-bearing mice, Par also exhibited an excellent anti-tumor effect, decreasing the tissue levels of P50 and HIF-1α.This study discovers that Par can inhibit the HIF-1α-mediated glycolysis of HCC cells by targeting P50, thereby exerting an anti-tumor effect. P50 is a major effective target of Par.</p>","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8346-8356"},"PeriodicalIF":5.2,"publicationDate":"2022-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9648796/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40343166","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lamin A to Z in normal aging.","authors":"Stanley R Primmer,&nbsp;Chen-Yu Liao,&nbsp;Oona M P Kummert,&nbsp;Brian K Kennedy","doi":"10.18632/aging.204342","DOIUrl":"https://doi.org/10.18632/aging.204342","url":null,"abstract":"<p><p>Almost since the discovery that mutations in the LMNA gene, encoding the nuclear structure components lamin A and C, lead to Hutchinson-Gilford progeria syndrome, people have speculated that lamins may have a role in normal aging. The most common HPGS mutation creates a splice variant of lamin A, progerin, which promotes accelerated aging pathology. While some evidence exists that progerin accumulates with normal aging, an increasing body of work indicates that prelamin A, a precursor of lamin A prior to C-terminal proteolytic processing, accumulates with age and may be a driver of normal aging. Prelamin A shares properties with progerin and is also linked to a rare progeroid disease, restrictive dermopathy. Here, we describe mechanisms underlying changes in prelamin A with aging and lay out the case that this unprocessed protein impacts normative aging. This is important since intervention strategies can be developed to modify this pathway as a means to extend healthspan and lifespan.</p>","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8150-8166"},"PeriodicalIF":5.2,"publicationDate":"2022-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9648802/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40343164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum adenosine deaminase activity and acute cerebral infarction: a retrospective case-control study based on 7913 participants.","authors":"Yanyan Ling,&nbsp;Chuan Jiang,&nbsp;Zhenzhen Xiao,&nbsp;Xiao Shang,&nbsp;Qi Li,&nbsp;Baojie Wang,&nbsp;Maolin Hao,&nbsp;Fei Liu,&nbsp;Nannan Zhao,&nbsp;Jianli Feng,&nbsp;Hongqin Zhao","doi":"10.18632/aging.204338","DOIUrl":"https://doi.org/10.18632/aging.204338","url":null,"abstract":"<p><strong>Background: </strong>Adenosine deaminase (ADA) is a key enzyme that catalyzes the deamination of adenosine into inosine, which eventually decomposes into uric acid (UA). A body of papers have reported that adenosine and UA are closely related to cerebrovascular events. However, the association between serum ADA activity and acute cerebral infarction (ACI) remains unclear.</p><p><strong>Methods: </strong>7913 subjects were enrolled, including 3968 ACI patients and 3945 controls, in this study. An automatic biochemistry analyzer was used to determine serum activity.</p><p><strong>Results: </strong>Serum ADA activity was found that was significantly decreased in patients with ACI (10.10 ± 3.72 U/L) compared to those without ACI (11.07 ± 2.85 U/L, <i>p</i> < 0.001). After Logistic regression analysis, ADA concentrations were negatively correlated with ACI (OR = 1.161, 95% CI: 1.140-1.183, <i>p</i> < 0.001). Smoking and alcohol consumption decreased serum ADA concentrations in patients with ACI, whereas diabetes and hypertension had the opposite effect.</p><p><strong>Conclusions: </strong>Serum ADA concentrations in patients with ACI are markedly decreased, suggesting that the decreased ADA concentrations may be involved in the pathogenesis of ACI. We hypothesized that decreased ADA activity may be an adaptive mechanism to maintain adenosine levels and protect against ischemic brain injury.</p>","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8719-8728"},"PeriodicalIF":5.2,"publicationDate":"2022-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699761/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40343162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction for: The miR-590-3p/CFHR3/STAT3 signaling pathway promotes cell proliferation and metastasis in hepatocellular carcinoma.","authors":"Zhongzhong Wan,&nbsp;Xingrun Li,&nbsp;Xinru Luo,&nbsp;Bofan Wang,&nbsp;Xiang Zhou,&nbsp;Ao Chen","doi":"10.18632/aging.204346","DOIUrl":"https://doi.org/10.18632/aging.204346","url":null,"abstract":"","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8139"},"PeriodicalIF":5.2,"publicationDate":"2022-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9596210/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33513982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction for: Hypoxia-preconditioned olfactory mucosa mesenchymal stem cells abolish cerebral ischemia/reperfusion-induced pyroptosis and apoptotic death of microglial cells by activating HIF-1α.","authors":"Yan Huang,&nbsp;Fengbo Tan,&nbsp;Yi Zhuo,&nbsp;Jianyang Liu,&nbsp;Jialin He,&nbsp;Da Duan,&nbsp;Ming Lu,&nbsp;Zhiping Hu","doi":"10.18632/aging.204321","DOIUrl":"https://doi.org/10.18632/aging.204321","url":null,"abstract":"1Key Laboratory of Protein Chemistry and Developmental Biology of Ministry of Education, College of Life Sciences, Hunan Normal University, Changsha 410081, Hunan, P.R. China 2Department of Neurosurgery, Second Affiliated Hospital of Hunan Normal University, Changsha 410003, Hunan, P.R. China 3Hunan Provincial Key Laboratory of Neurorestoration, Second Affiliated Hospital of Hunan Normal University, Changsha 410003, Hunan, P.R. China 4Department of Gastrointestinal Surgery, Xiangya Hospital, Central South University, Changsha 410008, Hunan, P.R. China 5Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha 410011, Hunan, P.R. China *Equal contribution","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8137-8138"},"PeriodicalIF":5.2,"publicationDate":"2022-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9596215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33513583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development and assessment of diabetic nephropathy prediction model using hub genes identified by weighted correlation network analysis.","authors":"Xuelian Zhang,&nbsp;Yao Wang,&nbsp;Zhaojun Yang,&nbsp;Xiaoping Chen,&nbsp;Jinping Zhang,&nbsp;Xin Wang,&nbsp;Xian Jin,&nbsp;Lili Wu,&nbsp;Xiaoyan Xing,&nbsp;Wenying Yang,&nbsp;Bo Zhang","doi":"10.18632/aging.204340","DOIUrl":"https://doi.org/10.18632/aging.204340","url":null,"abstract":"<p><p>Diabetic nephropathy (DN) is one microvascular complication of diabetes. About 30% of diabetic patients can develop DN, which is closely related to the high incidence and mortality of heart diseases, and then develop end-stage renal diseases. Therefore, early detection and screening of high-risk patients with DN is important. Herein, we explored the differences of serum transcriptomics between DN and non-DN in type II diabetes mellitus (T2DM) patients. We obtained 110 target genes using weighted correlation network analysis. Gene Ontology enrichment analysis indicates these target genes are mainly related to membrane adhesion, alpha-amino acid biosynthesis, metabolism, and binding, terminus, inhibitory synapse, clathrinid-sculpted vesicle, kinase activity, hormone binding, receptor activity, and transporter activity. Kyoto Encyclopedia of Genes and Genomes analysis indicates the process of DN in diabetic patients can involve synaptic vesicle cycle, cysteine and methionine metabolism, N-Glycan biosynthesis, osteoclast differentiation, and cAMP signaling pathway. Next, we detected the expression levels of hub genes in a retrospective cohort. Then, we developed a risk score tool included in the prediction model for early DN in T2DM patients. The prediction model was well applied into clinical practice, as confirmed by internal validation and several other methods. A novel DN risk model with relatively high prediction accuracy was established based on clinical characteristics and hub genes of serum detection. The estimated risk score can help clinicians develop individualized intervention programs for DN in T2DM. External validation data are required before individualized intervention measures.</p>","PeriodicalId":503342,"journal":{"name":"Aging","volume":" ","pages":"8095-8109"},"PeriodicalIF":5.2,"publicationDate":"2022-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9596198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33512422","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}