Molecular medicine reports最新文献

{"title":"Role and clinical value of serum hsa_tsr011468 in lung adenocarcinoma.","authors":"Ping Zhao, Kui Zhu, Cuihua Xie, Sinan Liu, Xiang Chen","doi":"10.3892/mmr.2024.13350","DOIUrl":"10.3892/mmr.2024.13350","url":null,"abstract":"<p><p>Transfer RNA‑derived small RNAs (tsRNAs) are novel non‑coding RNAs that are associated with the pathogenesis of various diseases. However, their association with lung adenocarcinoma (LUAD) has not been studied comprehensively. Therefore, the present study aimed to explore the diagnostic value of a tsRNA, hsa_tsr011468, in LUAD. The OncotRF database was used to screen tsRNAs and reverse transcription‑quantitative PCR (RT‑qPCR) was performed to detect the expression levels of hsa_tsr011468 in various samples. Subsequently, the diagnostic and prognostic values of hsa_tsr011468 for LUAD were determined via receiver operating characteristic (ROC) curve and survival curve analyses, and by assessing clinicopathological parameters. In addition, both nuclear and cytoplasmic RNA were extracted to assess the location of hsa_tsr011468. The OncotRF database identified high expression of hsa_tsr011468 in LUAD. In addition, the results of RT‑qPCR showed that the relative expression levels of hsa_tsr011468 in the serum and tissues of patients with LUAD were higher than those in normal controls. Furthermore, its expression was lower in postoperative serum samples than in preoperative serum samples from patients with LUAD. ROC and survival curves indicated that hsa_tsr011468 had good diagnostic and prognostic value. Furthermore, the clinicopathological analysis revealed that hsa_tsr011468 was associated with tumor size. In addition, hsa_tsr011468 was mainly localized in the cytoplasm of LUAD cells. The present study indicated that hsa_tsr011468 has good diagnostic value and, therefore, could be employed as a serum marker for LUAD.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11485271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142372282","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}

{"title":"[Corrigendum] Zoledronic acid sensitizes breast cancer cells to fulvestrant via ERK/HIF‑1 pathway inhibition <i>in vivo</i>.","authors":"Xiaoqing Jia, Jingyi Cheng, Zhenzhou Shen, Zhimin Shao, Guangyu Liu","doi":"10.3892/mmr.2024.13357","DOIUrl":"10.3892/mmr.2024.13357","url":null,"abstract":"<p><p>Following the publication of the above article, the authors drew to the Editor's attention that they had inadvertently used the same immunohistochemical image to show the experiments depicting the zoledronic acid‑treated MCF‑7/HIF‑1α xenograft (the 'ZOL/MCF‑7/hif' panel) and the fulvestrant‑treated MCF‑7/vector xenograft (the 'FUL/MCF‑7/cdh' panel) in Fig. 3A on p. 5474. Subsequently, upon performing an independent review of the data in this paper, the Editorial Office pointed out to the authors that the same colony‑formation assay image had been included in Fig. 1C to show the 'MCF‑7/cdh‑ZOL' and 'MCF‑7/cdh‑FUL' experiments. The authors re‑examined their original data, and realized that inadvertent errors were made during the compilation of this pair of figures. The corrected versions of Figs. 1 and 3 are shown on the next two pages, now featuring the correct data for the 'MCF‑7/cdh‑ZOL' experiment in Fig. 1C and the 'ZOL/MCF‑7/hif' experiment in Fig. 3A. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of <i>Molecular Medicine Reports</i> for granting them the opportunity to publish this. Furthermore, they regret that these errors were introduced into the paper, even though they did not substantially alter any of the major conclusions reported in the paper, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 17: 5470‑5476, 2018; DOI: 10.3892/mmr.2018.8514].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400775","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}

{"title":"[Retracted] ANRIL is associated with the survival rate of patients with colorectal cancer, and affects cell migration and invasion  <i>in</i> <i>vitro</i>.","authors":"Yi Sun, Zhao-Peng Zheng, Hang Li, Han-Qun Zhang, Fa-Qiang Ma","doi":"10.3892/mmr.2024.13354","DOIUrl":"10.3892/mmr.2024.13354","url":null,"abstract":"<p><p>Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the Transwell migration and invasion assay data shown in Fig. 4A and B on p. 1418 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had already been published elsewhere prior to the submission of this paper to <i>Molecular Medicine Reports</i>. In view of the fact that the abovementioned data had already apparently been published previously, the Editor of <i>Molecular Medicine Reports</i> has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports  14: 1714‑1720, 2016; DOI: 10.3892/mmr.2016.5409].</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11475094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142400776","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}

{"title":"Exosomal miR‑194 from adipose‑derived stem cells impedes hypertrophic scar formation through targeting TGF‑β1.","authors":"Zhishan Xu, Yuan Tian, Lijun Hao","doi":"10.3892/mmr.2024.13340","DOIUrl":"10.3892/mmr.2024.13340","url":null,"abstract":"<p><p>Hypertrophic scars, which result from aberrant fibrosis and disorganized collagen synthesis by skin fibroblasts, emerge due to disrupted wound healing processes. These scars present significant psychosocial and functional challenges to affected individuals. The current treatment limitations largely arise from an incomplete understanding of the underlying mechanisms of hypertrophic scar development. Recent studies, however, have shed light on the potential of exosomal non‑coding RNAs interventions to mitigate hypertrophic scar proliferation. The present study assessed the impact of exosomes derived from adipose‑derived stem cells (ADSCs‑Exos) on hypertrophic scar formation using a rabbit ear model. It employed hematoxylin and eosin staining, Masson's trichrome staining and immunohistochemical staining techniques to track scar progression. The comprehensive analysis of the present study encompassed the differential expression of non‑coding RNAs, enrichment analyses of functional pathways, protein‑protein interaction studies and micro (mi)RNA‑mRNA interaction investigations. The results revealed a marked alteration in the expression levels of long non‑coding RNAs and miRNAs following ADSCs‑Exos treatment, with little changes observed in circular RNAs. Notably, miRNA (miR)‑194 emerged as a critical regulator within the signaling pathways that govern hypertrophic scar formation. Dual‑luciferase assays indicated a significant reduction in the promoter activity of TGF‑β1 following miR‑194 overexpression. Reverse transcription‑quantitative PCR and immunoblotting assays further validated the decrease in TGF‑β1 expression in the treated samples. In addition, the treatment resulted in diminished levels of inflammatory markers IL‑1β, TNF‑α and IL‑10. <i>In vivo</i> evidence strongly supported the role of miR‑194 in attenuating hypertrophic scar formation through the suppression of TGF‑β1. The present study endorsed the strategic use of ADSCs‑Exos, particularly through miR‑194 modulation, as an effective strategy for reducing scar formation and lowering pro‑inflammatory and fibrotic indicators such as TGF‑β1. Therefore, the present study advocated the targeted application of ADSCs‑Exos, with an emphasis on miR‑194 modulation, as a promising approach to managing proliferative scarring.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465438/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350369","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}

{"title":"Therapeutic role of histone deacetylase inhibition in an <i>in vitro</i> model of Graves' orbitopathy.","authors":"Hyeong Ju Byeon, Soo Hyun Choi, Don O Kikkawa, Jaesang Ko, Jin Sook Yoon","doi":"10.3892/mmr.2024.13342","DOIUrl":"10.3892/mmr.2024.13342","url":null,"abstract":"<p><p>Graves' orbitopathy (GO), a manifestation of Graves' disease, is characterized by orbital fibroblast‑induced inflammation, leading to fibrosis or adipogenesis. Histone deacetylase (HDAC) serves a central role in autoimmune diseases and fibrosis. The present study investigated HDAC inhibition in orbital fibroblasts from patients with GO to evaluate its potential as a therapeutic agent. Primary cultured orbital fibroblasts were treated with an HDAC inhibitor, panobinostat, under the stimulation of IL‑1β, TGF‑β or adipogenic medium. Inflammatory cytokines, and fibrosis‑ and adipogenesis‑related proteins were analyzed using western blotting. The effects of panobinostat on HDAC mRNA expression were measured in GO orbital fibroblasts, and specific HDACs were inhibited using small interfering RNA transfection. Panobinostat significantly reduced the IL‑1β‑induced production of inflammatory cytokines and TGF‑β‑induced production of fibrosis‑related proteins. It also suppressed adipocyte differentiation and adipogenic transcription factor production. Furthermore, it significantly attenuated HDAC7 mRNA expression in GO orbital fibroblasts. In addition, the silencing of HDAC7 led to anti‑inflammatory and anti‑fibrotic effects. In conclusion, by inhibiting HDAC7 gene expression, panobinostat may suppress the production of inflammatory cytokines, profibrotic proteins and adipogenesis in GO orbital fibroblasts. The present <i>in vitro</i> study suggested that HDAC7 could be a potential therapeutic target for inhibiting the inflammatory, adipogenic and fibrotic mechanisms of GO.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465418/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142350370","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}

{"title":"Advances in research on the relationship between the LMNA gene and human diseases (Review).","authors":"Jiumei Zhao, Huijuan Zhang, Chenglong Pan, Qian He, Kepu Zheng, Yu Tang","doi":"10.3892/mmr.2024.13358","DOIUrl":"10.3892/mmr.2024.13358","url":null,"abstract":"<p><p>The LMNA gene, which is responsible for encoding lamin A/C proteins, is recognized as a primary constituent of the nuclear lamina. This protein serves crucial roles in various cellular physiological activities, including the maintenance of cellular structural stability, regulation of gene expression, mechanosensing and cellular motility. A significant association has been established between the LMNA gene and several major human diseases. Mutations, dysregulated expression of the LMNA gene, and improper processing of its encoded protein can result in a spectrum of pathological conditions. These diseases, collectively termed laminopathies, are directly attributed to LMNA gene dysfunction. The present review examines the recent advancements in research concerning the LMNA gene and its association with human diseases, while exploring its pathological roles. Particular emphasis is placed on the current status of LMNA gene research in the context of tumors. This includes an analysis of the abundance of LMNA alterations in cancer and its interplay with various signaling pathways. The aim of the present review was to provide novel perspectives for studying the development of LMNA‑related diseases and additional theoretical insights for basic and clinical translational research in this field.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470262","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}

{"title":"Cytoglobin attenuates melanoma malignancy but protects melanoma cells from ferroptosis.","authors":"Zuquan Zou, Qingyao Yu, Yong Yang, Feng Wang, Pan Zhu, Xiaohong Zhang, Jinjie Zhang","doi":"10.3892/mmr.2024.13343","DOIUrl":"10.3892/mmr.2024.13343","url":null,"abstract":"<p><p>Cutaneous malignant melanoma is the most aggressive and the deadliest form of skin cancer. There are two types of limitations which universally exist in current melanoma therapy: Adverse effects and reduced efficiency. Cytoglobin (CYGB), an iron hexacoordinated globin, is highly enriched in melanocytes and frequently epigenetically silenced during melanoma genesis. The present study aimed to explore its potential role as a biomarker for ferroptosis treatment. It was observed that B16F10 and A375 melanoma cells with loss of CYGB expression were highly sensitive to ferroptosis inducers RSL3 and erastin, whereas G361 melanoma cells with highly enriched CYGB were resistant to RSL3 or erastin. Ectopically overexpressed CYGB rendered B16F10 and A375 cells resistant to RSL3 or erastin, accompanied by decreased proliferation and epithelial‑mesenchymal transition (EMT). By contrast, knockdown of CYGB expression made G361 cells sensitive to ferroptosis induction but induced proliferation and EMT progression of G361 cells. Mechanistically, CYGB‑induced resistance of melanoma cells to ferroptosis may have been associated, in part, with i) Suppression of EMT; ii) upregulation of glutathione peroxidase 4 expression; iii) decrease of labile iron pool. <i>In vivo</i> study also demonstrated that CYGB overexpression rendered xenograft melanoma much more resist to RSL3 treatment. Based on these findings, CYGB is a potential therapeutic biomarker to screen the melanoma patients who are most likely benefit from ferroptosis treatment.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11465429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381278","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}

{"title":"Exploring the anti‑oxidative mechanisms of <i>Rhodiola rosea</i> in ameliorating myocardial fibrosis through network pharmacology and <i>in vitro</i> experiments.","authors":"Luna Zhang, Hang Yin, Yumin Xie, Yueyue Zhang, Feihong Dong, Ke Wu, Le Yang, Huiyi Lv","doi":"10.3892/mmr.2024.13338","DOIUrl":"10.3892/mmr.2024.13338","url":null,"abstract":"<p><p>Myocardial fibrosis (MF) significantly compromises cardiovascular health by affecting cardiac function through excessive collagen deposition. This impairs myocardial contraction and relaxation and leads to severe complications and increased mortality. The present study employed network pharmacology and <i>in vitro</i> assays to investigate the bioactive compounds of <i>Rhodiola rosea</i> and their targets. Using databases such as HERB, the Encyclopedia of Traditional Chinese Medicine, Pubchem, OMIM and GeneCards, the present study identified effective components and MF‑related targets. Network analysis was conducted with Cytoscape to develop a Drug‑Ingredient‑Target‑Disease network and the STRING database was utilized to construct a protein‑protein interaction network. Key nodes were analyzed for pathway enrichment using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. Molecular interactions were further explored through molecular docking techniques. The bioactivity of salidroside (SAL), the principal component of <i>Rhodiola rosea</i>, against MF was experimentally validated in H9c2 cardiomyocytes treated with angiotensin II and assessed for cell viability, protein expression and oxidative stress markers. Network pharmacology identified 25 active ingredients and 372 targets in <i>Rhodiola rosea</i>, linking SAL with pathways such as MAPK, EGFR, advanced glycosylation end products‑advanced glycosylation end products receptor and Forkhead box O. SAL showed significant interactions with core targets such as albumin, IL6, AKT serine/threonine kinase 1, MMP9 and caspase‑3. <i>In vitro</i>, SAL mitigated AngII‑induced increases in collagen I and alpha smooth muscle actin protein levels and oxidative stress markers, demonstrating dose‑dependent effectiveness in reversing MF. SAL from <i>Rhodiola rosea</i> exhibited potent anti‑oxidative properties that mitigated MF by modulating multiple molecular targets and signaling pathways. The present study underscored the therapeutic potential of SAL in treating oxidative stress‑related cardiovascular diseases.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11450433/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381280","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}

{"title":"MUC1‑ND interacts with TRPV1 to promote corneal epithelial cell proliferation in diabetic dry eye mice by partly activating the AKT signaling pathway.","authors":"Haiqiong Li, Yu Zhang, Yuting Chen, Rong Zhu, Weikang Zou, Hui Chen, Jia Hu, Songfu Feng, Yanyan Zhong, Xiaohe Lu","doi":"10.3892/mmr.2024.13337","DOIUrl":"10.3892/mmr.2024.13337","url":null,"abstract":"<p><p>Although both mucin1 (MUC1) and transient receptor potential cation channel subfamily V member 1 (TRPV1) have been reported to be associated with dry eye (DE) disease, whether they interact and their regulatory roles in diabetic DE disease are unknown. Diabetic DE model mice were generated by streptozotocin induction and assessed by corneal fluorescein staining, tear ferning (TF) tests, phenol red thread tests, hematoxylin and eosin staining of corneal sections and periodic acid Schiff staining of conjunctival sections. Cell proliferation was measured by CCK8 assay. Western blotting was performed to measure protein expression. Primary mouse corneal epithelial cells (MCECs) were cultured after enzymatic digestion. Immunofluorescence staining of MCECs and frozen corneal sections was conducted to assess protein expression and colocalization. Coimmunoprecipitation was performed to detect protein‑protein interactions. It was found that, compared with control mice, diabetic DE mice exhibited increased corneal epithelial defects, reduced tear production, poorer TF pattern grades and impaired corneal and conjunctival tissues. <i>In vivo</i> and <i>in vitro</i> experiments showed that hyperglycemia impaired cell proliferation, accompanied by decreased levels of the MUC1 extracellular domain (MUC1‑ND) and TRPV1. Additionally, it was found that capsazepine (a TRPV1 antagonist) inhibited the proliferation of MCECs. Notably, MUC1‑ND was shown to interact with the TRPV1 protein in the control group but not in the diabetic DE group. It was also found that the AKT signaling pathway was attenuated in the diabetic DE mice and downstream of TRPV1. MUC1‑ND interacted with TRPV1, partly activating the AKT signaling pathway to promote MCEC proliferation. The present study found that the interaction of MUC1‑ND with TRPV1 promotes MCEC proliferation by partly activating the AKT signaling pathway, providing new insight into the pathogenesis of corneal epithelial dysfunction in diabetic DE disease.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11450431/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142381282","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}

{"title":"Irisin improves ROS‑induced mitohormesis imbalance in H9c2 cells.","authors":"Baogui Wang, Haibo Xu, Shuai Shang, Longxiang Liu, Chunlong Sun, Wen Du","doi":"10.3892/mmr.2024.13364","DOIUrl":"10.3892/mmr.2024.13364","url":null,"abstract":"<p><p>Abnormal mitohormesis is a key pathogenic mechanism that induces a variety of cardiac diseases, including cardiac hypertrophy and heart failure. Irisin as a muscle factor serves a cardioprotective role in response to cellular oxidative stress injury. Rat cardiomyocyte cells (H9c2) were treated with 40 µM exogenous H₂O₂ to establish an oxidative stress model, followed by addition of 75 nM exogenous irisin for experiments to determine mitochondrial membrane potential, reactive oxygen species, and Mitohormesis‑related factors by attrition cytometry. Subsequently, the expression of mitochondrial membrane potential, reactive oxygen species and Mitohormesis‑related factors were continued to be determined by establishing a peroxisome proliferator‑activated receptor γ coactivator‑1 alpha (PGC‑1α) siRNA interference model and continuing the treatment with the addition of 75 nM irisin 12 h before the end of interference. When H9c2 cells underwent oxidative stress, irisin partially improved mitochondrial membrane potential and reactive oxygen species levels and partially restored mitochondrial energy metabolism by upregulating fusion proteins optic atrophy 1 (OPA1) mitochondrial dynamin‑like GTPase and mitofusin 2 and downregulating fission protein dynamin‑related protein 1. Following interference with PGC‑1α, irisin promoted mitochondrial biosynthesis by increasing the mRNA levels of OPA1 and protein levels of cytochrome c oxidase subunit 4. These results suggested that irisin acted partially independently of the PGC‑1α signaling pathway to regulate mitohormesis imbalance due to oxidative stress and maintain energy metabolism by improving mitochondrial structure.</p>","PeriodicalId":18818,"journal":{"name":"Molecular medicine reports","volume":"30 6","pages":""},"PeriodicalIF":3.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11544398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470265","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}