International journal of molecular medicine最新文献

{"title":"Understanding the impact of mitochondrial DNA mutations on aging and carcinogenesis (Review).","authors":"Hiroshi Kobayashi, Shogo Imanaka","doi":"10.3892/ijmm.2025.5559","DOIUrl":"10.3892/ijmm.2025.5559","url":null,"abstract":"<p><p>Mitochondria and mitochondrial DNA (mtDNA) are crucial for cellular energy metabolism and the adaptive response to environmental changes. mtDNA collaborates with the nuclear genome to regulate mitochondrial function. Dysfunctional mitochondria and mutations in mtDNA are implicated in a wide range of diseases, including mitochondrial disorders, neurodegenerative conditions, age‑associated pathologies and cancer. While the nuclear genome has been extensively studied for its role in driving the clonal expansion of oncogenes and other aging‑related genetic alterations, knowledge regarding mtDNA remains comparatively limited. However, advances in quantitative analysis have provided information regarding the complex patterns of mtDNA mutations. The present review offers a detailed examination of mtDNA mutations and their classifications in the contexts of aging and cancer, and elucidates the role of mtDNA mutations in these processes. Mutations in mtDNA can be detected as early as the neonatal stage, yet most transition mutations retain a normal cellular phenotype. In contrast to mutations in oncogenes and tumor suppressor genes within the nuclear genome, mtDNA exhibits conserved mutational signatures, irrespective of cancer tissue origin. To adapt to the aging process, mitochondria undergo clonal expansion of advantageous mtDNA mutations, maintaining a dynamic equilibrium among various mitochondrial clones. Over time, however, the loss of strand bias can disrupt this equilibrium, diminishing the pool of adaptive clones. This breakdown in mitochondrial homeostasis may contribute to tumorigenesis. In conclusion, the heterogeneity of mtDNA mutations and the collapse of its homeostasis are pivotal in the progression of age‑related diseases, including cancer, underscoring the importance of mtDNA mutations in health and disease.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234034","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":"Epigenetic roles of chromatin remodeling complexes in bone biology and the pathogenesis of bone‑related disease (Review).","authors":"Wenxiao Wu, Yinxing Cui, Yuqi Wu, Yan Ni, Chunling Zhao, Weichao Sun, Qian Yi","doi":"10.3892/ijmm.2025.5556","DOIUrl":"10.3892/ijmm.2025.5556","url":null,"abstract":"<p><p>Chromatin remodeling complexes are essential regulators of chromatin architecture, facilitating critical processes such as nucleosome sliding, eviction, histone exchange and post‑translational modifications. By providing an additional layer of epigenetic regulation beyond the canonical genetic code, these complexes significantly influence bone biology and health. Epigenetic regulation through chromatin remodeling complexes is crucial in modulating gene expression and cellular behavior in bone cells. However, alterations in the activity of chromatin remodeling complexes can also contribute to the progression of various bone diseases. Emerging evidence suggests that specific chromatin remodeling factors may serve as potential biomarkers for diagnosing bone‑related conditions and as therapeutic targets for intervention. The present review aims to elucidate the intricate relationship between chromatin remodeling complexes and bone‑related diseases, including osteoporosis, osteoarthritis and osteosarcoma. The present review discusses the diverse subunits of these complexes and their multifaceted roles in regulating key cellular processes such as stemness, differentiation, proliferation, senescence and apoptosis in bone cells. Notably, the present review provides a comprehensive overview of the roles of various chromatin remodeling subunits, such as BRG1, BAF47 and chromodomain‑helicase‑DNA binding 7 (CHD7), in bone metabolism, highlighting their disease‑specific mechanisms, including bromodomain‑containing protein (BRD)9‑mediated pyroptosis in intervertebral disc degeneration and CHD7‑driven bone‑fat imbalance. Furthermore, the present review highlights the therapeutic potential of targeting dysfunctional subunits (such as BRD7 in osteosarcoma and SS18 in synovial sarcoma) and propose AI‑driven structural biology approaches to design chemical modulators. The understudied impact of aging on chromatin remodeling activity in bone homeostasis is also underscored, advocating for longitudinal studies to address this gap. Finally, the distinct functions of each chromatin remodeling complex and its specific subunits in the context of bone‑related diseases were also explored, providing a comprehensive understanding of their contributions to both normal bone physiology and pathological conditions.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144180502","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":"The regulatory role of CDK4/6 inhibitors in tumor immunity and the potential value of tumor immunotherapy (Review).","authors":"Feifan He, Qiuchen Zhang, Yunjie Chen, Suli Ge, Yidai Xie, Ruihong Sun, Yuqing Wu, Jian Xu","doi":"10.3892/ijmm.2025.5564","DOIUrl":"10.3892/ijmm.2025.5564","url":null,"abstract":"<p><p>Cyclin‑dependent kinase (CDK)4/6 inhibitors regulate the cell cycle by binding to CDK4/6, thus exerting an inhibitory effect, and they have a notable impact on tumor immunity. CDK4/6 inhibitors have been demonstrated to modulate the immune microenvironment by affecting immune cells and immune escape phenomena in the tumor microenvironment. T cells, natural killer cells and macrophages are all regulated by CDK4/6 inhibitors, thereby acting on cancer cells. In addition, these inhibitors modulate immune checkpoints, enhancing antitumor immune responses when combined with immune checkpoint inhibitors, such as programmed death‑ligand 1 and programmed death‑1. However, these inhibitors are not without limitations, as they can enhance tumor immune evasion. Therefore, combination therapies to improve efficacy are being investigated, including immunotherapy, targeted therapy, chemotherapy and radiation therapy. In addition, challenges associated with the widespread use of CDK4/6 inhibitors, such as the emergence of tumor resistance, underscore the necessity for further research to enhance the clinical applicability of these inhibitors.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176271/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144283856","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":"Insight into microbial extracellular vesicles as key communication materials and their clinical implications for lung cancer (Review).","authors":"Jeong Yun Jang, Ji Hoon Seo, Jae Jun Choi, Hyun Jin Ryu, Hyunjun Yun, Dong Myeong Ha, Jinho Yang","doi":"10.3892/ijmm.2025.5560","DOIUrl":"10.3892/ijmm.2025.5560","url":null,"abstract":"<p><p>The complexity of lung cancer, driven by multifactorial causes such as genetic, environmental and lifestyle factors, underscores the necessity for tailored treatment strategies informed by recent advancements. Studies highlight a significant association between the lung microbiome and lung cancer, with dysbiosis potentially contributing to disease development via inflammation, immune response alterations and bacterial metabolite production. Furthermore, exposure to airborne bacteria may influence lung health by introducing pathogenic species or altering the human microbiome, thereby implicating certain dominant airborne bacteria in lung diseases, including the exacerbation of lung cancer. Extracellular vesicles (EVs) facilitate cell‑to‑cell communication, penetrating mucosal barriers to impact various organs, notably the lung. Epidemiological evidence suggests a strong relationship between the presence of microbial EVs (MEVs) in the air and chronic pulmonary diseases, with indications of a potential risk for lung cancer. MEVs play a significant role in pulmonary disease development by inducing airway inflammation and affecting lung function. The microbiome and MEVs offer considerable potential as novel tools in precision medicine for lung cancer. Biological data analysis and artificial intelligence technology advancements are pivotal for fully realizing their diagnostic and therapeutic capabilities. These developments can potentially shape the future landscape of lung cancer diagnostics, therapeutics and prevention strategies.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234030","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":"Cell migration in diabetic wound healing: Molecular mechanisms and therapeutic strategies (Review).","authors":"Jielin Song, Tong Zhao, Chuanfu Wang, Xu Sun, Junchao Sun, Zhaohui Zhang","doi":"10.3892/ijmm.2025.5567","DOIUrl":"10.3892/ijmm.2025.5567","url":null,"abstract":"<p><p>Diabetic wounds are among the most prevalent forms of chronic wound and are a prominent clinical challenge in contemporary healthcare. Impaired cell migration represents one of the key mechanisms underlying the difficulty in diabetic wound healing, involving multiple cell types including neutrophils, macrophages, keratinocytes, endothelial cells and fibroblasts. Under the influence of pathological factors, including hyperglycemia, chronic inflammation, oxidative stress and an abnormal microenvironment, the cell migration becomes impaired, leading to delayed wound healing. Key signaling pathways including Rho GTPase, PI3K/Akt, TGF‑β/Smad and Wnt/β‑catenin are involved in the regulation of cell migration. Non‑coding RNAs exert a pivotal influence on diabetic wound healing by modulating these signaling pathways or their downstream targets. Notably, stem cells and their exosomes, growth factor therapy, drug‑loaded dressings and traditional Chinese medicine can modulate cell migration via non‑coding RNAs and associated signaling pathways, thereby establishing a therapeutic regulatory axis. This review systematically consolidates advances in this field, providing novel insight into the mechanisms of cell migration in diabetic wounds and facilitating the development of innovative therapeutic strategies.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12180913/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333093","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] Morin exerts cytoprotective effects against oxidative stress in C2C12 myoblasts via the upregulation of Nrf2‑dependent HO‑1 expression and the activation of the ERK pathway.","authors":"Moon Hee Lee, Min Ho Han, Dae-Sung Lee, Cheol Park, Su-Hyun Hong, Gi-Young Kim, Sang Hoon Hong, Kyoung Seob Song, Il-Whan Choi, Hee-Jae Cha, Yung Hyun Choi","doi":"10.3892/ijmm.2025.5555","DOIUrl":"10.3892/ijmm.2025.5555","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that the β‑actin blots in Figs. 4B and 5B were apparently the same, even though different experimental conditions were reported for these figure parts; moreover, the data shown as the Lamin B blot in Fig. 5A had also been incorporated as the Akt data in Fig. 5C of a different paper submitted by the same group and published in the journal <i>Oncology Reports</i>. However, the authors were able to re‑examine their data, and realized how these errors had occurred. Upon repeating the experiments relating to the affected figure parts, which resulted in the generation of similar results, revised versions of Figs. 4 and 5, now including replacement data for Fig. 4A and Fig. 5A and B, are shown on the next page. Note that the errors made with the assembly of the data in these figures did not affect the overall conclusions reported in the paper. The authors are grateful to have been given the opportunity to publish this corrigendum, and all the authors agree with its publication; furthermore, they apologize to the Editor of <i>International Journal of Molecular Medicine</i> and to the readership for any inconvenience caused. [International Journal of Molecular Medicine 39: 399‑406, 2017; DOI: 10.3892/ijmm.2016.2837].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12140092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144181525","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":"Relationship between amino acid metabolism and inflammation in coronary heart disease (Review).","authors":"Ruxin Shen, Yingying Zhang","doi":"10.3892/ijmm.2025.5561","DOIUrl":"10.3892/ijmm.2025.5561","url":null,"abstract":"<p><p>This review delves into the intricate relationship between amino acid metabolism and inflammation in coronary heart disease (CHD). Research shows that disruptions in the metabolism of arginine, glutamate, branched‑chain amino acids (BCAAs) and tryptophan exacerbate CHD inflammation via immunometabolic reprogramming and oxidative stress. Nitric oxide (NO), produced from arginine metabolism, regulates CHD progression multifacetedly. Glutamate metabolism dysregulation harms cardiovascular health, while glutamine exerts cardioprotective effects after myocardial infarction. Elevated BCAA levels are associated with atherosclerosis development, and tryptophan and its metabolites have complex effects on CHD. Notably, amino acid metabolism intersects with the immune system, modulating the functions of T cells, B cells and macrophages. These immune cells are crucial for CHD‑related inflammation. Inflammatory markers like high‑sensitivity C‑reactive protein, interleukin family members, interferon‑γ and monocyte chemoattractant protein‑1 are closely linked to CHD pathogenesis and progression, facilitating risk assessment. Clinical research, including animal and human studies, and technological applications such as metabolomics, offer insights into CHD diagnosis, treatment and prevention. Dietary intervention and drug therapy targeting amino acid metabolism show potential. For example, L‑arginine supplementation has cardioprotective effects and novel NO donors like compound‑N6 hold promise. However, certain substances like triclocarban have adverse impacts, while colchicine is beneficial. In summary, while current research has advanced the understanding of CHD, significant knowledge gaps remain, particularly regarding rare amino acids and the connection between amino acid metabolism and non‑coding RNA. Future research could utilize metabolomics, genomics and artificial intelligence for personalized CHD management, representing a paradigm shift towards individualized precision medicine.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 2","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12176267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234032","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] Predictive DNA damage signaling for low‑dose ionizing radiation.","authors":"Jeong-In Park, Seung-Youn Jung, Kyung-Hee Song, Dong-Hyeon Lee, Jiyeon Ahn, Sang-Gu Hwang, In-Su Jung, Dae-Seog Lim, Jie-Young Song","doi":"10.3892/ijmm.2025.5553","DOIUrl":"10.3892/ijmm.2025.5553","url":null,"abstract":"<p><p>Following the publication of the above article, the authors drew to the Editor's attention that two pairs of the data panels shown for the flow cytometric experiments in Fig. 3B on p. 7 had inadvertently been duplicated in the figure, such that these data were derived from the same original source, even though they were intended to have shown the results from different experiments. The authors were able to consult their original data, however, and the revised version of Fig. 3, now containing the correctly assembled flow cytometric plots in Fig. 3B, is shown on the next page. Note that the errors made in assembling these figures did not affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for granting them the opportunity to publish this. Furthermore, they apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 53: 56, 2024; DOI: 10.3892/ijmm.2024.5380].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12121982/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142150","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":"Application of liquid biopsy in differentiating lung cancer from benign pulmonary nodules (Review).","authors":"Mingcheng Peng, Jun Gong, Taixue An, Hongbing Cheng, Liangji Chen, Mengyang Cai, Jinhua Lan, Yueting Tang","doi":"10.3892/ijmm.2025.5547","DOIUrl":"10.3892/ijmm.2025.5547","url":null,"abstract":"<p><p>The diagnosis of malignant and benign pulmonary nodules has always been a prominent research topic. Accurately distinguishing between these types of lesions, particularly small or ground glass nodules, is crucial for the early detection and proactive treatment of lung cancer, ultimately leading to improved patient survival. Although various imaging methods and tissue biopsies have advanced the diagnostic efficacy of pulmonary nodules, each approach possesses inherent limitations. In recent years, there has been a growing interest in liquid biopsy as a non‑invasive and easily obtainable alternative. Furthermore, in‑depth investigations into the mechanisms underlying tumor initiation and progression have contributed to the development of circulating biomarkers for monitoring treatment response and efficacy in lung cancer. This review provides a comprehensive overview of the current landscape of pulmonary nodule diagnosis while highlighting the latest advancements in liquid biopsy techniques, such as extracellular vesicles, tumor‑educated platelets, non‑coding RNA, circulating tumor DNA and circulating antibodies.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101102/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143993337","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":"miR‑34a induces apoptosis and pyroptosis in D‑Galactose‑induced aging cochlear hair cells via inhibiting TFAM and promoting mitochondrial dysfunction <i>in vitro</i> and <i>in vivo</i>.","authors":"Yilan Wang, Ming Yang, Guihua Wang, Weimin Liu, Bin Deng, Xiaoran Yang, Xuzhao Li","doi":"10.3892/ijmm.2025.5541","DOIUrl":"10.3892/ijmm.2025.5541","url":null,"abstract":"<p><p>Aging of the auditory system causes progressive hearing deficit and affects millions of people; however, the underlying mechanism remains largely unknown. D‑galactose (D‑gal)‑induced aging models were established <i>in vitro</i> using HEI‑OC1 cells and <i>in vivo</i> using C57BL/6 mice to investigate the role of miR‑34a in age‑related hearing loss (ARHL). HEI‑OC1 cells were treated with D‑gal for, while mice received daily intraperitoneal injections of D‑gal for six weeks. Molecular and functional analyses, including reverse transcription‑quantitative PCR, Western blot, flow cytometry, immunofluorescence, and dual‑luciferase reporter assays, were performed to evaluate oxidative stress, mitochondrial dysfunction, apoptosis, and pyroptosis, with miR‑34a inhibitor and DRP1 inhibitor (Mdivi‑1) used to assess their regulatory effects. D‑gal induced hair cell loss by apoptosis and pyroptosis, which was modulated by microRNA (miR)‑34a via mitochondrial dysfunction <i>in vitro</i> and <i>in vivo</i>. Inhibition of mitochondrial transcription factor A (TFAM), which is the target gene of miR‑34a, was involved in the underlying molecular mechanism. miR‑34a mediated apoptosis and pyroptosis in D‑gal‑induced cochlear hair cells via inhibiting TFAM and promoting mitochondrial dysfunction <i>in vitro</i> and <i>in vivo</i> and may serve as a new potential target for future ARHL treatment.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"56 1","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12081035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143980825","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}