International journal of molecular medicine最新文献

{"title":"Thymoquinone mitigates cardiac hypertrophy by activating adaptive autophagy via the PPAR‑γ/14‑3‑3γ pathway.","authors":"Rong-Bin Qiu, Shi-Tao Zhao, Zhi-Qiang Xu, Li-Juan Hu, Rui-Yuan Zeng, Zhi-Cong Qiu, Han-Zhi Peng, Lian-Fen Zhou, Yuan-Ping Cao, Li Wan","doi":"10.3892/ijmm.2025.5500","DOIUrl":"10.3892/ijmm.2025.5500","url":null,"abstract":"<p><p>Thymoquinone (TQ), the principal active compound derived from the black seed plant, has been extensively utilized in traditional medicine for treating various ailments. Despite its widespread use, its therapeutic mechanisms in the context of cardiac hypertrophy remain insufficiently understood. The present study focused on assessing the efficacy of TQ in mitigating cardiac hypertrophy while identifying its specific protective pathways. Through a combination of <i>in vivo</i> experiments utilizing a mouse model of transverse aortic constriction (TAC) and <i>in vitro</i> studies utilizing an angiotensin II (AngII)‑induced hypertrophy model in H9C2 cells, the protective actions of TQ were comprehensively evaluated. The results revealed that TQ significantly attenuated TAC‑induced cardiac hypertrophy and improved overall cardiac function. In AngII‑induced H9C2 cells, pretreatment with TQ significantly reduced both cell hypertrophy and reactive oxygen species levels, while simultaneously promoting autophagy and limiting fibrosis. TQ was also found to increase the transcriptional activity of peroxisome proliferator‑activated receptor‑γ (PPAR‑γ), which interacted with 14‑3‑3γ protein, leading to autophagy activation and subsequent cellular protection. However, the protective autophagic effects were attenuated when PPAR‑γ activity was inhibited alongside pAD/14‑3‑3γ‑short hairpin RNA administration. The present findings demonstrate that TQ mitigates cardiac hypertrophy by modulating autophagy via the PPAR‑γ/14‑3‑3γ signaling axis, highlighting its therapeutic potential for cardiac hypertrophy treatment.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 4","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878483/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143364669","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] Morroniside protects SK‑N‑SH human neuroblastoma cells against H₂O₂‑induced damage.","authors":"Jing-Xing Zhang, Rui Wang, Jin Xi, Lin Shen, An-You Zhu, Qi Qi, Qi-Yi Wang, Lun-Jun Zhang, Feng-Chao Wang, He-Zuo Lü, Jian-Guo Hu","doi":"10.3892/ijmm.2025.5501","DOIUrl":"10.3892/ijmm.2025.5501","url":null,"abstract":"<p><p>Following the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 2D on p. 606, which showed the results of cellular morphological experiments, two pairs of data panels were overlapping, such that data which were intended to show the results obtained under different experimental conditions may have been derived from the same original sources. The authors examined their original data, and realized that this figure had been assembled incorrectly (they were also able to send the data underlying this figure on to the Editorial Office for our inspection). The revised version of Fig. 2, now showing alternative data from one set of the repeated experiments, is shown on the next page. The authors confirm that the errors associated with this figure did not have any significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of <i>International Journal of Molecular Medicine</i> for granting them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 39: 603‑612, 2017; DOI: 10.3892/ijmm.2017.2882].</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 4","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143412939","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":"Elevated neuregulin‑1 expression modulates tumor malignancy and autophagy in esophageal squamous cell carcinoma.","authors":"Yen-Chiang Tseng, Pei-Feng Liu, Yu-Ru Chen, Wen-Hsin Yang, Chia-Che Chang, Hsueh-Wei Chang, Cheng-Hsin Lee, Yih-Gang Goan, Chih-Wen Shu","doi":"10.3892/ijmm.2025.5503","DOIUrl":"10.3892/ijmm.2025.5503","url":null,"abstract":"<p><p>The 5‑year survival rate of patients with esophageal squamous cell carcinoma (ESCC) is <20%, highlighting the need for the development of novel therapeutic targets. Neuregulin‑1 (NRG1), a transmembrane protein involved in cell proliferation and survival signaling, has unclear biological functions and clinical value in ESCC. The present study investigated the association between NRG1 expression and ESCC by analyzing data from both patients with ESCC and The Cancer Genome Atlas database. Reverse transcription‑quantitative PCR and immunohistochemistry staining were used to determine the levels of gene and protein in the tissue. The findings revealed that NRG1 gene and protein levels were significantly higher in tumor tissues compared with the normal tissues. Elevated expression of NRG1 was associated with poor outcomes, particularly in patients with advanced ESCC. Silencing NRG1 decreased both its mRNA and protein levels, disrupting key signaling pathways, such as phosphorylated (p‑)AKT and cellular rapidly accelerated fibrosarcoma (p‑cRAF), which led to decreased cancer cell proliferation, migration and tumor sphere formation, along with increased cell death. High expression levels of NRG1 and cRAF were significantly associated with poor prognosis. Additionally, silencing NRG1 promoted autophagosome and autolysosome formation, decreasing LC3B levels. The use of the autophagy inhibitor chloroquine significantly enhanced cell death induced by NRG1 silencing, suggesting that autophagy functions as a survival mechanism in ESCC cells in which NRG1 is silenced. Furthermore, high co‑expression of NRG1 and LC3B was associated with a worse prognosis. On the whole, the present study demonstrated that targeting NRG1 with autophagy inhibitors may serve as a potential therapeutic strategy for ESCC.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 4","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11878479/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143413224","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":"Recent insights and perspectives into the role of the miRNA‑29 family in innate immunity (Review).","authors":"Xing-Chen Yao, Jun-Jie Wu, Sheng-Tao Yuan, Feng-Lai Yuan","doi":"10.3892/ijmm.2025.5494","DOIUrl":"10.3892/ijmm.2025.5494","url":null,"abstract":"<p><p>Innate immunity is the first line of defence against pathogenic microorganisms and is nearly universal among eukaryotes. The innate immune system is composed of various organs, cells and immune molecules. MicroRNAs (miRs) are a class of small non‑coding RNAs (~22 nucleotides) that are widely involved in post‑transcriptional regulation of proteins within the innate immune system through the recognition of seed sequences. The present review summarizes the role of the miR‑29 family in innate immunity, with a focus on its specific functions in the differentiation of T cells, B cells, natural killer cells and macrophages, as well as the mechanisms by which the miR‑29 family participates in innate immune signalling. Additionally, this review discusses how the miR‑29 family helps the host combat infections by hepatitis B and C viruses, human immunodeficiency virus and influenza A virus through the regulation of specific signalling molecules. This comprehensive analysis of existing studies emphasizes the importance of the miR‑29 family in maintaining immune balance and defence against pathogens.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781520/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065458","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":"Curcumin attenuates myocardial ischemia‑reperfusion‑induced autophagy‑dependent ferroptosis via Sirt1/AKT/FoxO3a signaling.","authors":"Shi-Tao Zhao, Zhi-Cong Qiu, Zhi-Qiang Xu, En-De Tao, Rong-Bin Qiu, Han-Zhi Peng, Lian-Fen Zhou, Rui-Yuan Zeng, Song-Qing Lai, Li Wan","doi":"10.3892/ijmm.2025.5492","DOIUrl":"10.3892/ijmm.2025.5492","url":null,"abstract":"<p><p>Curcumin (Cur) effectively attenuates myocardial ischemia/reperfusion injury (MIRI). MIRI has a complex mechanism and is associated with autophagy‑dependent ferroptosis. Therefore, the present study aimed to determine whether autophagy‑dependent ferroptosis occurs in MIRI and assess the mechanism of Cur in attenuating MIRI. The study was conducted on a Sprague‑Dawley rat MIRI model and H9c2 cell anoxia/reoxygenation (A/R) injury model. The effect of Cur pretreatment on A/R or MIRI induced autophagy‑dependent ferroptosis and its molecular mechanism were investigated. Protein expression, lysosomal, reactive oxygen species, Fe2+, oxidative systems, mitochondrial function, subcellular localization of molecules, and cardiac function assays will be employed. Cur decreased MIRI; improved myocardial histopathology; increased cardiomyocyte viability; inhibited ferroptosis, apoptosis and autophagy; reduced infarct size and maintained cardiac function. MIRI decreased silent information regulator 1 (Sirt1), decreased AKT and forkhead box O3A (FoxO3a) phosphorylation, leading to FoxO3a entry into the nucleus to activate translation of autophagy‑related genes and inducing ferroptosis, apoptosis and autophagy. However, Cur pretreatment activated AKT and FoxO3a phosphorylation via Sirt1, thereby transporting FoxO3a out of the nucleus, reducing autophagy‑related gene translation and attenuating MIRI‑induced ferroptosis, apoptosis and autophagy. Of note, the silencing of Sirt1 and administration of triciribine (an AKT inhibitor) both eliminated the protective effect of Cur. Thus, Cur maintained cardiomyocyte function by inhibiting autophagy‑dependent ferroptosis via Sirt1/AKT/FoxO3a signaling.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390904","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":"RGS12 is a target of penehyclidine hydrochloride that enhances oxidative stress and ferroptosis in a model of myocardial ischemia/reperfusion injury by inhibiting the Nrf2 pathway.","authors":"Congna Zi, Yulei Wei, Ying Zhu, Juan Fan","doi":"10.3892/ijmm.2025.5493","DOIUrl":"10.3892/ijmm.2025.5493","url":null,"abstract":"<p><p>Regulator of G‑protein signaling 12 (RGS12) is a regulatory factor that is involved in various physiological processes. However, the role of RGS12 in myocardial ischemia/reperfusion injury (MIRI) currently remains unclear. The present study established a mouse model of MIRI by ligating the left main coronary artery followed by reperfusion. In addition, mouse HL‑1 cells were cultured in a hypoxic and serum‑free medium, followed by reoxygenation to establish an <i>in vitro</i> cell model of hypoxia/reoxygenation (H/R). Adenoviruses targeting RGS12 were subsequently used to either overexpress or silence RGS12 expression. RGS12 was highly expressed in both the myocardial tissues of mice with MIRI and HL‑1 cells subjected to H/R. The results from the <i>in vitro</i> experiments demonstrated that the knockdown of RGS12 reduced oxidative stress under a pathological environment, as indicated by decreased reactive oxygen species (ROS) levels and malondialdehyde activity and increased activities of superoxide dismutase and catalase. Furthermore, mice with MIRI and HL‑1 cells that underwent H/R stimulation exhibited increased ferroptosis, whereas RGS12 knockdown reversed these changes. These results showed that post‑RGS12 silencing the levels of Fe²⁺ and lipid ROS were decreased, the expression levels of glutathione peroxidase 4 and cystine transporter solute carrier family 7 member 11 were increased and mitochondrial structure was improved by preventing the loss of the mitochondrial crest. Mechanistically, the nuclear factor erythroid 2‑related factor 2 (Nrf2) pathway with anti‑ferroptosis and anti‑oxidative stress capacities was activated by RGS12 knockdown. Conversely, RGS12 overexpression exerted the opposite effects both in vivo and in vitro. Notably, it was demonstrated that penehyclidine hydrochloride (PHC), known to block the MIRI process, decreased RGS12 expression levels both <i>in vivo</i> and <i>in vitro</i>, and RGS12 overexpression inhibited the therapeutic effects of PHC on MIRI. In conclusion, the present study demonstrated that RGS12, a target of PHC, potentially enhanced the progression of MIRI by promoting oxidative stress and ferroptosis, and this effect may involve the regulation of the Nrf2 pathway.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781519/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390906","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":"NLRP3 inflammasome in health and disease (Review).","authors":"Haoran Wang, Li Ma, Weiran Su, Yangruoyu Liu, Ning Xie, Jun Liu","doi":"10.3892/ijmm.2025.5489","DOIUrl":"10.3892/ijmm.2025.5489","url":null,"abstract":"<p><p>Activation of inflammasomes is the activation of inflammation‑related caspase mediated by the assembly signal of multi‑protein complex and the maturity of inflammatory factors, such as IL‑1β and IL‑18. Among them, the Nod‑like receptor family pyrin domain containing 3 (NLRP3) inflammasome is the most thoroughly studied type of inflammatory corpuscle at present, which is involved in the occurrence and development of numerous human diseases. Therefore, targeting the NLRP3 inflammasome has become the focus of drug development for related diseases. In this paper, the research progress of the NLRP3 inflammasome in recent years is summarized, including the activation and regulation of NLRP3 and its association with diseases. A deep understanding of the regulatory mechanism of NLRP3 will be helpful to the discovery of new drug targets and the development of therapeutic drugs.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781521/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390905","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":"Research progress on the molecular mechanisms of Saikosaponin D in various diseases (Review).","authors":"Simin Gu, Yiyuan Zheng, Chong Chen, Jing Liu, Yanping Wang, Junmin Wang, Yong Li","doi":"10.3892/ijmm.2024.5478","DOIUrl":"10.3892/ijmm.2024.5478","url":null,"abstract":"<p><p>Bupleurum, a Traditional Chinese Medicine (TCM) herb, is widely used in China and other Asian countries to manage chronic liver inflammation and viral hepatitis. Saikosaponin D (SSD), a triterpenoid saponin extracted from Bupleurum, exhibits extensive pharmacological properties, including anti‑inflammatory, antioxidant, anti‑apoptotic, anti‑fibrotic and anti‑cancer effects, making it a therapeutic candidate for numerous diseases. Clarifying the targets and molecular mechanisms underlying TCM compounds is essential for scientifically validating TCM's therapeutic roles in disease prevention and treatment, as well as for identifying novel therapeutic targets and lead compounds. This analysis comprehensively examines SSD's mechanisms across various conditions, such as myocardial injury, pulmonary diseases, hepatic disorders, renal pathologies, neurological disorders, diabetes and cancer. In addition, challenges and potential solutions encountered in SSD research are addressed. SSD is posited as a promising monomer for multifaceted therapeutic applications and this article aims to enhance researchers' understanding of the current landscape of SSD studies, offering strategic insights to guide future investigations.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11722148/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142880955","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":"Protective role of triiodothyronine in sepsis‑induced cardiomyopathy through phospholamban downregulation.","authors":"Qiumin Xie, Qin Yi, Jing Zhu, Bin Tan, Han Xiang, Rui Wang, Huiwen Liu, Tangtian Chen, Hao Xu","doi":"10.3892/ijmm.2025.5488","DOIUrl":"10.3892/ijmm.2025.5488","url":null,"abstract":"<p><p>Sepsis is often a cause of mortality in patients admitted to the intensive care unit. Notably, the heart is the organ most susceptible to the impact of sepsis and this condition is referred to as sepsis‑induced cardiomyopathy (SIC). Low triiodothyronine (T3) syndrome frequently occurs in patients with sepsis, and the heart is one of the most important target organs for the action of T3. Phospholamban (PLN) is a key protein associated with Ca²⁺‑pump‑mediated cardiac diastolic function in the myocardium of mice with SIC, and PLN is negatively regulated by T3. The present study aimed to explore whether T3 can protect cardiac function during sepsis and to investigate the specific molecular mechanism underlying the regulation of PLN by T3. C57BL/6J mice and H9C2 cells were used to establish <i>in vivo</i> and <i>in vitro</i> models, respectively. Myocardial damage was detected via pathological tissue sections, a Cell Counting Kit-8 assay, an apoptosis assay and crystal violet staining. Intracellular calcium levels and reactive oxygen species were detected by Fluo‑4AM and DHE fluorescence. The protein and mRNA expression levels of JNK and c‑Jun were measured by western blotting and reverse transcription‑quantitative PCR to investigate the molecular mechanisms involved. Subsequently, 100 clinical patients were recruited to verify the clinical application value of PLN in SIC. The results revealed a significant negative correlation between PLN and T3 in the animal disease model. Furthermore, the expression levels of genes and proteins in the JNK/c‑Jun signaling pathway and PLN expression levels were decreased, whereas the expression levels of sarcoplasmic reticulum calcium ATPase were increased after T3 treatment. These results indicated that T3 alleviated myocardial injury in SIC by inhibiting PLN expression and its phosphorylation, which may be related to the JNK/c‑Jun signaling pathway. Accordingly, PLN may have clinical diagnostic value in patients with SIC.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11781518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143005158","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":"Iron metabolism and the tumor microenvironment: A new perspective on cancer intervention and therapy (Review).","authors":"Xiaorui Bu, Lufang Wang","doi":"10.3892/ijmm.2024.5480","DOIUrl":"10.3892/ijmm.2024.5480","url":null,"abstract":"<p><p>Iron metabolism plays a crucial role in the tumor microenvironment, influencing various aspects of cancer cell biology and tumor progression. This review discusses the regulatory mechanisms of iron metabolism within the tumor microenvironment and highlights how tumor cells and associated stromal cells manage iron uptake, accumulation and regulation. The sources of iron within tumors and the biological importance of ferroptosis in cancer were explored, focusing on its mechanisms, biological effects and, in particular, its tumor‑suppressive properties. Furthermore, the protective strategies employed by cancer cells to evade ferroptosis were examined. This review also delves into the intricate relationship between iron metabolism and immune modulation within the tumor microenvironment, detailing the impact on tumor‑associated immune cells and immune evasion. The interplay between ferroptosis and immunotherapy is discussed and potential strategies to enhance cancer immunotherapy by modulating iron metabolism are presented. Finally, the current ferroptosis‑based cancer therapeutic approaches were summarized and future directions for therapies that target iron metabolism were proposed.</p>","PeriodicalId":14086,"journal":{"name":"International journal of molecular medicine","volume":"55 3","pages":""},"PeriodicalIF":5.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11722052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142921597","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}