Molecular medicine reports最新文献_第2页

Silencing of ERRα gene represses cell proliferation and induces apoptosis in human skin fibroblasts. 沉默ERRα基因可抑制人皮肤成纤维细胞的增殖并诱导其凋亡。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-10-25 DOI: 10.3892/mmr.2024.13370

Naoki Nanashima, Toshio Norikura, Manabu Nakano, Chie Hata, Kayo Horie

{"title":"Silencing of ERRα gene represses cell proliferation and induces apoptosis in human skin fibroblasts.","authors":"Naoki Nanashima, Toshio Norikura, Manabu Nakano, Chie Hata, Kayo Horie","doi":"10.3892/mmr.2024.13370","DOIUrl":"10.3892/mmr.2024.13370","url":null,"abstract":"Estrogen‑related receptor (ERR) is an orphan nuclear receptor structurally akin to the estrogen receptor. ERR is expressed in tissues with active energy metabolism and regulates intracellular metabolic functions. Additionally, ERRs are known to be strongly expressed in the epidermis of skin tissue, but their functions are unknown. The present study investigated the function of ERRα in human skin fibroblasts. ERRα expressed in human dermal fibroblast TIG113 was knocked down using small interfering (si)RNA and gene expression was comprehensively analyzed using microarrays 48 h later. Pathway analysis was performed using Wikipathways on genes exhibiting expression changes of ≥1.5‑fold. Expression of cell cycle‑related and apoptosis‑related genes was compared using reverse transcription‑quantitative PCR. After treating TIG113 cells with siERRα for 72 h, cell proliferation was assessed using the Cell Counting Kit‑8 or a scratch wound healing assay and apoptotic cells were measured using the Poly Caspase Assay Kit. Cell cycle analysis was performed using flow cytometry. The expression of the ERRα gene was suppressed by siRNA. The expression of genes associated with cell cycle‑related pathways were decreased while that of those associated with apoptosis‑related pathways increased. Furthermore, the expression of cell cycle‑related genes such as cell division cycle 25C, cyclin E and cyclin B1 was decreased and the expression of apoptosis‑related genes such as caspase3 and Fas cell surface death receptor was increased. Cell proliferation was suppressed and the number of apoptotic cells increased ~2‑fold in ERRα‑knockdown TIG113 cells. Cell cycle analysis revealed that the number of cells in the Sub‑G1 phase increased and that in the S and G2/M phases decreased. The present study suggested that ERRα is an essential for the survival of human skin fibroblasts.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Selective protein degradation through chaperone‑mediated autophagy: Implications for cellular homeostasis and disease (Review). 通过伴侣介导的自噬选择性降解蛋白质：对细胞稳态和疾病的影响（综述）。

IF 4.3 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-11-08 DOI: 10.3892/mmr.2024.13378

Jiahui Huang, Jiazhen Wang

{"title":"Selective protein degradation through chaperone‑mediated autophagy: Implications for cellular homeostasis and disease (Review).","authors":"Jiahui Huang, Jiazhen Wang","doi":"10.3892/mmr.2024.13378","DOIUrl":"10.3892/mmr.2024.13378","url":null,"abstract":"Cells rely on autophagy for the degradation and recycling of damaged proteins and organelles. Chaperone-mediated autophagy (CMA) is a selective process targeting proteins for degradation through the coordinated function of molecular chaperones and the lysosome‑associated membrane protein‑2A receptor (LAMP2A), pivotal in various cellular processes from signal transduction to the modulation of cellular responses under stress. In the present review, the intricate regulatory mechanisms of CMA were elucidated through multiple signaling pathways such as retinoic acid receptor (RAR)α, AMP‑activated protein kinase (AMPK), p38‑TEEB‑NLRP3, calcium signaling‑NFAT and PI3K/AKT, thereby expanding the current understanding of CMA regulation. A comprehensive exploration of CMA's versatile roles in cellular physiology were further provided, including its involvement in maintaining protein homeostasis, regulating ferroptosis, modulating metabolic diversity and influencing cell cycle and proliferation. Additionally, the impact of CMA on disease progression and therapeutic outcomes were highlighted, encompassing neurodegenerative disorders, cancer and various organ‑specific diseases. Therapeutic strategies targeting CMA, such as drug development and gene therapy were also proposed, providing valuable directions for future clinical research. By integrating recent research findings, the present review aimed to enhance the current understanding of cellular homeostasis processes and emphasize the potential of targeting CMA in therapeutic strategies for diseases marked by CMA dysfunction.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11542157/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604600","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Gut‑liver axis in liver disease: From basic science to clinical treatment (Review). 肝病中的肠肝轴：从基础科学到临床治疗（综述）。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-10-25 DOI: 10.3892/mmr.2024.13375

Jianpeng Wang, Xinyi Wang, Enba Zhuo, Bangjie Chen, Shixin Chan

引用次数: 0

Long non‑coding RNA SNHG1 promotes autophagy in vascular smooth muscle cells induced by facilitating CLEC7A. 长非编码 RNA SNHG1 在促进 CLEC7A 的诱导下促进血管平滑肌细胞的自噬。

IF 4.3 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-11-08 DOI: 10.3892/mmr.2024.13385

Hao-Wei Deng, Wen-Bin Teng, Shao-Dan Zhou, Zi-Ming Ye, Zi-Mei Dong, Rui-Ting Hu, Chao Qin

{"title":"Long non‑coding RNA SNHG1 promotes autophagy in vascular smooth muscle cells induced by facilitating CLEC7A.","authors":"Hao-Wei Deng, Wen-Bin Teng, Shao-Dan Zhou, Zi-Ming Ye, Zi-Mei Dong, Rui-Ting Hu, Chao Qin","doi":"10.3892/mmr.2024.13385","DOIUrl":"10.3892/mmr.2024.13385","url":null,"abstract":"Long non‑coding RNAs serve a crucial role in autophagy of vascular smooth muscle cells (VSMCs). The present study aimed to investigate the effect of small nucleolar RNA host gene 1 (SNHG1) on autophagy in VSMCs and the associated underlying mechanisms. Rapamycin was used to induce autophagy in VSMCs and the effects of SNHG1 on the proliferation and migration of VSMCs and the change in phenotype were tested following overexpression and silencing of SNHG1. The target gene of SNHG1 was predicted and validated. SNHG1‑regulated autophagy of VSMCs via C‑type lectin domain family 7 member A (CLEC7A) was determined by combined silencing of SNHG1 and overexpression of CLEC7A. Rapamycin‑induced autophagy in VSMCs changed the cell phenotype from contractile to synthetic, with decreased expression of α‑smooth muscle actin and smooth muscle protein 22a and increased expression of osteopontin. Overexpression of SNHG1 caused the same change in phenotype while the opposite change was observed following SNHG1 silencing. Overexpression of SNHG1 promoted the proliferation and migration of VSMCs. CLEC7A was identified as a target gene of SNHG1 and a direct binding relationship between them was confirmed by RNA immunoprecipitation and RNA pull‑down assays. Overexpression of SNHG1 increased the expression of CLEC7A. The expression of both SNHG1 and CLEC7A was increased during autophagy of VSMCs. Overexpression of SNHG1 promoted autophagy of VSMCs and silencing of CLEC7A reduced this effect of SNHG1. In conclusion, SNHG1 and CLEC7A were increased in VSMCs following autophagy. SNHG1 promotes the conversion of VSMCs from a contractile phenotype to a synthetic phenotype by facilitating CLEC7A expression.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11564905/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

[Corrigendum] Effect of STC2 gene silencing on colorectal cancer cells. [更正] STC2 基因沉默对结直肠癌细胞的影响。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-11-08 DOI: 10.3892/mmr.2024.13386

Qianyuan Li, Xiukou Zhou, Zhengyu Fang, Zhiyun Pan

{"title":"[Corrigendum] Effect of STC2 gene silencing on colorectal cancer cells.","authors":"Qianyuan Li, Xiukou Zhou, Zhengyu Fang, Zhiyun Pan","doi":"10.3892/mmr.2024.13386","DOIUrl":"https://doi.org/10.3892/mmr.2024.13386","url":null,"abstract":"Subsequently to the publication of the above paper, an interested reader drew to the authors' attention that the 'Control' and 'NC' data panels shown in Fig. 2E on p. 981, showing the results of Transwell invasion assay experiments, appeared to contain overlapping sections of data, such that they were potentially derived from the same original source where these panels were intended to show the results from differently performed experiments. After having asked the authors to provide an explanation of these data, they realized that this figure had been inadvertently assembled incorrectly. A revised version of Fig. 2, containing replacement data for the experiments portrayed in Fig. 2E, is shown on the next page. Note that these errors did not adversely affect either the results or the overall conclusions reported in this study. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of Molecular Medicine Reports for allowing them the opportunity to publish this. They also wish to apologize to the readership of the Journal for any inconvenience caused. [Molecular Medicine Reports 20: 977‑984, 2019; DOI: 10.3892/mmr.2019.10332].","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142605526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

S100A16 stabilizes the ITGA3‑mediated ECM‑receptor interaction pathway to drive the malignant properties of lung adenocarcinoma cells via binding MOV10. S100A16 通过结合 MOV10 稳定 ITGA3 介导的 ECM-受体相互作用途径，从而驱动肺腺癌细胞的恶性特性。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-10-25 DOI: 10.3892/mmr.2024.13376

Lianren Yang, Ajuan Shen, Rujun Wang, Zhihui Zheng

{"title":"S100A16 stabilizes the ITGA3‑mediated ECM‑receptor interaction pathway to drive the malignant properties of lung adenocarcinoma cells via binding MOV10.","authors":"Lianren Yang, Ajuan Shen, Rujun Wang, Zhihui Zheng","doi":"10.3892/mmr.2024.13376","DOIUrl":"10.3892/mmr.2024.13376","url":null,"abstract":"Lung adenocarcinoma (LUAD) is highly associated with lung cancer‑associated mortality. Notably, S100 calcium‑binding protein A16 (S100A16) has been increasingly considered to have prognostic value in LUAD; however, the underlying mechanism remains unknown. In the present study, S100A16 expression levels in LUAD tissues and cells were respectively analyzed by the UALCAN database and western blotting. Cell Counting Kit‑8 and 5‑ethynyl‑2'‑deoxyuridine assays were used to examine cell proliferation, whereas wound healing, Transwell and tube formation assays were used to assess cell migration, invasion and angiogenesis, respectively. Western blotting was also used to examine the expression levels of proteins associated with metastasis, angiogenesis, focal adhesion and the extracellular matrix (ECM)‑receptor interaction pathways. The relationship between S100A16 and Mov10 RNA helicase (MOV10) was predicted by bioinformatics tools, and was verified using a co‑immunoprecipitation assay. Furthermore, the interaction between MOV10 and integrin α3 (ITGA3) was verified by RNA immunoprecipitation assay, and the actinomycin D assay was used to detect ITGA3 mRNA stability. The results demonstrated that S100A16 expression was increased in LUAD tissues and cell lines, and was associated with unfavorable outcomes. Knocking down S100A16 expression hindered the proliferation, migration, invasion and angiogenesis of LUAD cells. Furthermore, S100A16 was shown to bind to MOV10 and positively modulate MOV10 expression in LUAD cells, while MOV10 overexpression partially reversed the suppressive role of S100A16 knockdown on the aggressive phenotypes of LUAD cells. Furthermore, it was demonstrated that S100A16 regulated the stability of ITGA3 mRNA via MOV10 to mediate ECM‑receptor interactions. In conclusion, S100A16 may bind to MOV10 to stabilize ITGA3 mRNA and regulate ECM‑receptor interactions, hence contributing to the malignant progression of LUAD.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11541165/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Upregulation of miR‑6747‑3p affects red blood cell lineage development and induces fetal hemoglobin expression by targeting BCL11A in β‑thalassemia. miR-6747-3p的上调通过靶向BCL11A影响β地中海贫血症患者的红细胞系发育并诱导胎儿血红蛋白的表达。

IF 4.3 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-10-25 DOI: 10.3892/mmr.2024.13372

Aixiang Lv, Meihuan Chen, Siwen Zhang, Wantong Zhao, Jingmin Li, Siyang Lin, Yanping Zheng, Na Lin, Liangpu Xu, Hailong Huang

{"title":"Upregulation of miR‑6747‑3p affects red blood cell lineage development and induces fetal hemoglobin expression by targeting BCL11A in β‑thalassemia.","authors":"Aixiang Lv, Meihuan Chen, Siwen Zhang, Wantong Zhao, Jingmin Li, Siyang Lin, Yanping Zheng, Na Lin, Liangpu Xu, Hailong Huang","doi":"10.3892/mmr.2024.13372","DOIUrl":"10.3892/mmr.2024.13372","url":null,"abstract":"In β‑thalassemia, excessive α‑globin chain impedes the normal development of red blood cells resulting in anemia. Numerous miRNAs, including miR‑6747‑3p, are aberrantly expressed in β‑thalassemia major (β‑TM), but there are no reports on the mechanism of miR‑6747‑3p in regulating red blood cell lineage development and fetal hemoglobin (HbF) expression. In the present study, RT‑qPCR was utilized to confirm miR‑6747‑3p expression in patients with β‑TM and the healthy controls. Electrotransfection was employed to introduce the miR‑6747‑3p mimic and inhibitor in both HUDEP‑2 and K562 cells, and red blood cell lineage development was evaluated by CCK‑8 assay, flow cytometry, Wright‑Giemsa staining and Benzidine blue staining. B‑cell lymphoma/leukemia 11A (BCL11A) was selected as a candidate target gene of miR‑6747‑3p for further validation through FISH assay, dual luciferase assay and Western blotting. The results indicated that miR‑6747‑3p expression was notably higher in patients with β‑TM compared with healthy controls and was positively related to HbF levels. Functionally, miR‑6747‑3p overexpression resulted in the hindrance of cell proliferation, promotion of cell apoptosis, facilitation of cellular erythroid differentiation and γ‑globin expression in HUDEP‑2 and K562 cells. Mechanistically, miR‑6747‑3p could specifically bind to the 546‑552 loci of BCL11A 3'‑UTR and induce γ‑globin expression. These data indicate that upregulation of miR‑6747‑3p affects red blood cell lineage development and induces HbF expression by targeting BCL11A in β‑thalassemia, highlighting miR‑6747‑3p as a potential molecular target for β‑thalassemia therapy.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529187/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142504401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Peroxisome proliferator‑activated receptor γ coactivator‑1α in heart disease (Review). 心脏病中的过氧化物酶体增殖激活受体γ辅助激活剂-1α（综述）。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-11-08 DOI: 10.3892/mmr.2024.13382

Siyu Sun, Huige Guo, Guohui Chen, Hui Zhang, Zhanrui Zhang, Xiulong Wang, Dongxu Li, Xuefang Li, Guoan Zhao, Fei Lin

{"title":"Peroxisome proliferator‑activated receptor γ coactivator‑1α in heart disease (Review).","authors":"Siyu Sun, Huige Guo, Guohui Chen, Hui Zhang, Zhanrui Zhang, Xiulong Wang, Dongxu Li, Xuefang Li, Guoan Zhao, Fei Lin","doi":"10.3892/mmr.2024.13382","DOIUrl":"10.3892/mmr.2024.13382","url":null,"abstract":"Heart disease (HD) is a general term for various diseases affecting the heart. An increasing body of evidence suggests that the pathogenesis of HD is closely related to mitochondrial dysfunction. Peroxisome proliferator‑activated receptor γ coactivator‑1α (PGC‑1α) is a transcriptional coactivator that plays an important role in mitochondrial function by regulating mitochondrial biogenesis, energy metabolism and oxidative stress. The present review shows that PGC‑1α expression and activity in the heart are controlled by multiple signaling pathways, including adenosine monophosphate‑activated protein kinase, sirtuin 1/3 and nuclear factor κB. These can mediate the activation or inhibition of transcription and post‑translational modifications (such as phosphorylation and acetylation) of PGC‑1α. Furthermore, it highlighted the recent progress of PGC‑1α in HD, including heart failure, coronary heart disease, diabetic cardiomyopathy, drug‑induced cardiotoxicity and arrhythmia. Understanding the mechanisms underlying PGC‑1α in response to pathological stimulation may prove to be beneficial in developing new ideas and strategies for preventing and treating HDs. Meanwhile, the present review explored why the opposite results occurred when PGC‑1α was used as a target therapy.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11551696/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142604303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Integrin β2 regulates titanium particle‑induced inflammation in macrophages: In vitro aseptic loosening model. 整合素β2调节钛颗粒诱导的巨噬细胞炎症：体外无菌性松动模型。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-11-14 DOI: 10.3892/mmr.2024.13390

Yue Shen, Haruna Nakajima, Junfeng Zhu, Weigang Wu

{"title":"Integrin β2 regulates titanium particle‑induced inflammation in macrophages: In vitro aseptic loosening model.","authors":"Yue Shen, Haruna Nakajima, Junfeng Zhu, Weigang Wu","doi":"10.3892/mmr.2024.13390","DOIUrl":"https://doi.org/10.3892/mmr.2024.13390","url":null,"abstract":"Aseptic loosening is a major complication of joint replacement surgery, characterized by periprosthetic osteolysis and chronic inflammation at the bone‑implant interface. Cells release chemokines, cytokines and other pro‑inflammatory substances that perpetuate inflammation reactions, while other particle‑stimulated macrophages promote osteoclastic bone resorption and impair bone formation. The present study investigated integrin and inflammatory cytokine expression patterns in RAW 264.7 cells treated with titanium (Ti) particles to elucidate the role of integrins in Ti particle‑mediated inflammatory osteolysis. Assessment was performed by reverse transcription‑quantitative PCR, western blotting, confocal immunofluorescence, flow cytometry and enzyme‑linked immunosorbent assays. Cell migration was evaluated by wound healing assay. It was found that Ti particles significantly induced integrin expression in RAW 264.7 cells, including upregulation of integrins β2 (CD18), aL (CD11a), aM (CD11b) and aX (CD11c). Ti particles also enhanced the expression of Toll‑like receptors (TLRs; TLR1, TLR2, TLR3 and TLR4) and triggered the release of inflammatory cytokines such as tumor necrosis factor α, interleukin (IL)‑1β, IL‑8 and IL‑12. Proteomics showed higher expression and activity levels of TLR2 and TLR4, along with their downstream signaling adaptors myeloid differentiation primary response protein 88 (MyD88) and Mal/TIR‑domain‑containing adapter protein (TIRAP), following Ti treatment. Additionally, Ti treatment significantly enhanced the migration rate of RAW 264.7 cells. The present findings indicated that Ti particles regulate the inflammatory response of RAW 264.7 cells in an in vitro aseptic loosening model by activating the TLR/TIRAP/MyD88 signaling pathway.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624174","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Epigenetic modifications associated to diabetic peripheral neuropathic pain (Review). 与糖尿病周围神经痛相关的表观遗传修饰（综述）。

IF 3.4 3区医学

Molecular medicine reports Pub Date : 2025-01-01 Epub Date: 2024-11-14 DOI: 10.3892/mmr.2024.13394

Tangqing Gao, Jingya Luo, Juanning Fan, Gu Gong, Haihong Yang

{"title":"Epigenetic modifications associated to diabetic peripheral neuropathic pain (Review).","authors":"Tangqing Gao, Jingya Luo, Juanning Fan, Gu Gong, Haihong Yang","doi":"10.3892/mmr.2024.13394","DOIUrl":"10.3892/mmr.2024.13394","url":null,"abstract":"The present review aimed to provide an update on the scientific progress of the role of epigenetic modifications on diabetic peripheral neuropathic pain (DPNP). DPNP is a devastating and troublesome complication of diabetes mellitus (DM), which affects one third of patients with DM and causes severe hyperalgesia and allodynia, leading to challenges in the treatment of these patients. The pathophysiology of DPNP is multifactorial and is not yet fully understood and treatment options for this disease are currently unsatisfactory. The underlying mechanisms and pathophysiology of DPNP have largely been explored in animal models and a mechanism‑derived approach might offer a potential therapeutic‑target for attenuating certain phenotypes of DPNP. Altered gene expression levels within the peripheral or central nervous systems (CNS) are a crucial mechanism of DPNP, however, the transcriptional mechanisms of these genes have not been fully elucidated. Epigenetic modifications, such as DNA methylation and histone modifications (methylation, acetylation, or phosphorylation), can alter gene expression levels via chromatin remodeling. Moreover, it has been reported that altering gene expression via epigenetic modifications within the peripheral or CNS, contributes to the changes in both pain sensitivity and pharmacological efficacy in DPNP. Therefore, the present review summarized the findings of relevant literature on the epigenetic alterations in DPNP and the therapeutic potential for targeting these alterations in the future treatment of this disease.","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"31 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624225","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0