MedComm最新文献

{"title":"Combining JAK Inhibitors with Immune Checkpoint Inhibitors: Overcoming Resistance in Cancer Treatment","authors":"Hai-Jing Zhong","doi":"10.1002/mco2.70141","DOIUrl":"https://doi.org/10.1002/mco2.70141","url":null,"abstract":"<p>Balancing acute inflammation and chronic inflammation is challenging in cancer immunotherapy while two recent groundbreaking studies published in <i>Science</i> have shown a promising strategy to address this challenge by combining Janus kinase (JAK) inhibitors with anti-PD-1 therapy [<span>1, 2</span>].</p><p>One of these studies, Zak et al. [<span>1</span>] assessed the efficacy of combining the anti-PD-1 antibody nivolumab with ruxolitinib in patients with relapsed or refractory Hodgkin lymphoma. Ruxolitinib, the first JAK inhibitor approved by US Food and Drug Administration, has proven to be clinically useful in treating graft-versus-host disease and myeloproliferative neoplasms [<span>3</span>]. The combination therapy in the classical Hodgkin lymphoma (CHL) trial demonstrated striking efficacy, achieving a best overall response rate of 53% (10 out of 19). All enrolled patients had previously failed checkpoint inhibitor therapy, with eligibility criteria specifically requiring patients to have exhibited refractory disease, relapsed disease, or stable disease. Notably, significant clinical responses were observed in these patients.</p><p>In another clinical trial focusing on metastatic non-small cell lung cancer (NSCLC), the combination of anti-PD-1 therapy (pembrolizumab) and itacitinib, a selective JAK1 inhibitor, demonstrated remarkable efficacy. This study, conducted by Mathew et al., reported an overall response rate of 67% among the 21 treatment-naïve metastatic NSCLC patients with tumor PD-L1 ≥50% [<span>2</span>]. This response rate significantly surpasses historical response rate of 44.8% to pembrolizumab monotherapy in NSCLC.</p><p>Immune checkpoint inhibitors (ICIs) are widely used as standard treatments for various cancer types; however, their overall response rate remains low across the broader patient population [<span>4</span>]. These two studies in NSCLC and Hodgkin lymphoma show how well the combination works to enhance ICI efficacy and overcome resistance mechanisms (Figure 1).</p><p>JAK inhibitors help address the mixed effects of interferon (IFN) signaling, which can both stimulate and suppress antitumor immunity. While IFNs are important for antiviral and antitumor activity, persistent IFN signaling can lead to immunosuppression and resistance to ICIs therapy. This was demonstrated in the NSCLC study, where patients who responded to JAK inhibitor itacitinib addition showed decreased inflammatory signaling and reduced IFN-stimulated gene expression. By carefully timing JAK inhibition, the treatment can block the immunosuppressive effects of chronic inflammation while preserving beneficial acute inflammatory responses that support antitumor immunity. In the Hodgkin lymphoma study, the combination of ruxolitinib and checkpoint inhibitors demonstrated a unique ability to preserve and even enhance essential T cell functions, including cytokine production and proliferation, while carefully modulating chronic IFN signaling w","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70141","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554602","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolic reprogramming in cancer and senescence","authors":"Yuzhu Zhang,&nbsp;Jiaxi Tang,&nbsp;Can Jiang,&nbsp;Hanxi Yi,&nbsp;Shu Guang,&nbsp;Gang Yin,&nbsp;Maonan Wang","doi":"10.1002/mco2.70055","DOIUrl":"https://doi.org/10.1002/mco2.70055","url":null,"abstract":"<p>The rising trend in global cancer incidence has caused widespread concern, one of the main reasons being the aging of the global population. Statistical data show that cancer incidence and mortality rates show a clear upward trend with age. Although there is a commonality between dysregulated nutrient sensing, which is one of the main features of aging, and metabolic reprogramming of tumor cells, the specific regulatory relationship is not clear. This manuscript intends to comprehensively analyze the relationship between senescence and tumor metabolic reprogramming; as well as reveal the impact of key factors leading to cellular senescence on tumorigenesis. In addition, this review summarizes the current intervention strategies targeting nutrient sensing pathways, as well as the clinical cases of treating tumors targeting the characteristics of senescence with the existing nanodelivery research strategies. Finally, it also suggests sensible dietary habits for those who wish to combat aging. In conclusion, this review attempts to sort out the link between aging and metabolism and provide new ideas for cancer treatment.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70055","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholesterol-27α-hydroxylase inhibitor nilvadipine can effectively treat cholestatic liver injury in adult offspring induced by prenatal dexamethasone exposure","authors":"Wen Hu,&nbsp;Jiayong Zhu,&nbsp;Qi Zhang,&nbsp;Xiaoqian Lu,&nbsp;Luting Yu,&nbsp;Bin Li,&nbsp;Liaobin Chen,&nbsp;Hui Wang","doi":"10.1002/mco2.70110","DOIUrl":"https://doi.org/10.1002/mco2.70110","url":null,"abstract":"<p>Prenatal dexamethasone exposure (PDE) can increase offspring susceptibility to various diseases. However, the pathogenesis and early prevention for PDE offspring prone to cholestatic liver injury have been unclear. In this study, we collected human umbilical cord blood from neonates with prenatal dexamethasone therapy, showing increased primary unconjugated bile acid levels in utero. PDE increased blood primary bile acid levels, enhanced endoplasmic reticulum stress, and led to cholestatic liver injury in adulthood in rats, which is accompanied by the persistent increase of H3K14ac level in cholesterol 27α-hydroxylase (CYP27A1) promoter and its expression before and after birth. In vitro, dexamethasone activates glucocorticoid receptors, binding to the CYP27A1 promoter, and promotes its transcriptional expression. Through the miR-450b-3p/SIRT1 pathway, it increased the H3K14ac level of the CYP27A1 promoter to enhance its transcription, which continues after birth. Finally, nilvadipine effectively reversed cholestatic liver injury induced by PDE. This study confirmed PDE could cause cholestatic liver injury, and innovatively proposed its early intervention target (CYP27A1) and effective drug (nilvadipine), providing a theoretical and experimental basis for guiding rational drug use during pregnancy, and preventing and treating the fetal-originated cholestatic liver injury.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70110","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143554293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liver Metastasis in Cancer: Molecular Mechanisms and Management","authors":"Wenchao Xu,&nbsp;Jia Xu,&nbsp;Jianzhou Liu,&nbsp;Nanzhou Wang,&nbsp;Li Zhou,&nbsp;Junchao Guo","doi":"10.1002/mco2.70119","DOIUrl":"https://doi.org/10.1002/mco2.70119","url":null,"abstract":"<p>Liver metastasis is a leading cause of mortality from malignant tumors and significantly impairs the efficacy of therapeutic interventions. In recent years, both preclinical and clinical research have made significant progress in understanding the molecular mechanisms and therapeutic strategies of liver metastasis. Metastatic tumor cells from different primary sites undergo highly similar biological processes, ultimately achieving ectopic colonization and growth in the liver. In this review, we begin by introducing the inherent metastatic-friendly features of the liver. We then explore the panorama of liver metastasis and conclude the three continuous, yet distinct phases based on the liver's response to metastasis. This includes metastatic sensing stage, metastatic stress stage, and metastasis support stage. We discuss the intricate interactions between metastatic tumor cells and various resident and recruited cells. In addition, we emphasize the critical role of spatial remodeling of immune cells in liver metastasis. Finally, we review the recent advancements and the challenges faced in the clinical management of liver metastasis. Future precise antimetastatic treatments should fully consider individual heterogeneity and implement different targeted interventions based on stages of liver metastasis.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70119","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143513825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Noninvasive Quantification of Hepatic Steatosis Using Ultrasound-Derived Fat Fraction (CHESS2303): A Prospective Multicenter Study","authors":"Yunlin Huang,&nbsp;Jia Li,&nbsp;Chuan Liu,&nbsp;Danlei Song,&nbsp;Chuanlong Zhu,&nbsp;Yongfeng Ren,&nbsp;Jiaojian Lv,&nbsp;Longfeng Jiang,&nbsp;Rong Shan,&nbsp;Hao Wang,&nbsp;Zhou Wang,&nbsp;Siqin Long,&nbsp;Fan Jiang,&nbsp;Xiang Xie,&nbsp;Liren Lu,&nbsp;Ruixiang Qi,&nbsp;Pengfei Rong,&nbsp;Chuxiao Shao,&nbsp;Wang Yao,&nbsp;Youfang Gao,&nbsp;Wenping Wang,&nbsp;Juan Cheng,&nbsp;Vincent Wai-Sun Wong,&nbsp;Ying Wang,&nbsp;Wai-Kay Seto,&nbsp;Yi Dong,&nbsp;Christoph F. Dietrich,&nbsp;Xiaolong Qi","doi":"10.1002/mco2.70123","DOIUrl":"https://doi.org/10.1002/mco2.70123","url":null,"abstract":"<p>Ultrasound-derived fat fraction (UDFF) is designed to assess the hepatic fat content quantitatively. A multicenter study that verifies the diagnostic performance of UDFF for detecting hepatic steatosis has not yet been reported. This study aimed to evaluate the performance of UDFF for diagnosing and grading hepatic steatosis. Participants referred for assessment of hepatic steatosis were prospectively recruited from eight hospitals. All participants underwent UDFF and magnetic resonance imaging proton density fat fraction (MRI-PDFF) examinations. MRI-PDFF was used as the reference for diagnosing hepatic steatosis. From January 2023 to July 2023, a total of 300 participants were included. The median body mass index was 25.4 kg/m² (interquartile range: 22.7–28.1). UDFF values were positively correlated with MRI-PDFF (<i>R</i> = 0.80, <i>p</i> &lt; 0.001). Using MRI-PDFF ≥ 5%, ≥ 15%, and ≥ 25% as the reference standard for detecting mild, moderate, and severe hepatic steatosis, the best cutoff values of UDFF were 7.6% (area under the receiver operating characteristic curves [AUC] = 0.90), 15.9% (AUC = 0.90), and 22.3% (AUC = 0.91), respectively. Thus, UDFF has excellent diagnostic performance in detecting and grading hepatic steatosis.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70123","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143513827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting WDPF domain of Hsp27 achieves a broad spectrum of antiviral","authors":"Mandi Wu,&nbsp;Wei Li,&nbsp;Houying Leung,&nbsp;Yiran Wang,&nbsp;Qianya Wan,&nbsp;Peiran Chen,&nbsp;Cien Chen,&nbsp;Yichen Li,&nbsp;Xi Yao,&nbsp;Ming-Liang He","doi":"10.1002/mco2.70032","DOIUrl":"https://doi.org/10.1002/mco2.70032","url":null,"abstract":"<p>Enterovirus A71 (EV-A71) is a positive-sense single-stranded RNA virus, which hijacks host proteins to benefit viral internal ribosome entry site (IRES)-dependent protein translation and further propagation. We demonstrated that serine 78 (S78) phosphorylation of Hsp27 is critical for Hsp27/hnRNP A1 relocalization upon EV-A71 infection. Here, we report that the deletion of WDPF and ACD domains disturbs subcellular localization of Hsp27, resulting in partial nuclear translocation. The domain deletion-induced Hsp27 nuclear translocation fails to direct hnRNP A1 translocation. The 2A^pro-induced IRES activity and viral replication are suppressed by the deletion of WDPF or ACD domain. Surprisingly, a peptide (WDPF) dramatically inhibits S78 phosphorylation. Therefore, hnRNP A1 translocation, viral IRES activity, and viral protein translation and propagation are all strongly suppressed by the WDPF peptide, but not by peptide without WDPFR sequence (ΔWDPF). Moreover, the WDPF peptide also has potent antiviral activity on other RNA virus (e.g., coronavirus HCoV-OC43) and DNA virus (e.g., HSV-1 and HBV). Peptide treatment with kinase inhibitor Sorafenib brings an additional inhibitory effect on HCoV-OC43 and HSV-1. Taken together, we uncover a crucial role of WDPF domain in S78 phosphorylation for EV-A71-induced hnRNP A1 nuclear translocation, IRES-dependent viral protein translation, and EV-A71 propagation. Our results explore a new path for target-based pan-antiviral strategy.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70032","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143490021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endoscopic Ultrasound-Guided Brachytherapy of Yttrium-90 Implantation Into Pancreas: A Dose-Escalation Pilot Study","authors":"Yuchong Zhao,&nbsp;Yilei Yang,&nbsp;Buchuan Zhang,&nbsp;Haochen Cui,&nbsp;Luyao Liu,&nbsp;Ronghua Wang,&nbsp;Yunfeng Han,&nbsp;Dongling Zhu,&nbsp;Wenliang Ma,&nbsp;Xinxing Zhang,&nbsp;Jinlin Wang,&nbsp;Si Xiong,&nbsp;Shuya Bai,&nbsp;Xiaohua Zhu,&nbsp;Bin Cheng","doi":"10.1002/mco2.70117","DOIUrl":"https://doi.org/10.1002/mco2.70117","url":null,"abstract":"<p>Intratumoral brachytherapy enables higher dose treatment and reduces damage to adjacent tissues. We first validated the feasibility and safety of endoscopic ultrasound (EUS)-guided Yttrium-90 (⁹⁰Y) microspheres implantation in a porcine model. Under EUS guidance, ⁹⁰Y-loaded microspheres were implanted into the pancreas of 10 miniature pigs. The first pig was implanted with 10 MBq particles. Subsequently, nine pigs were sequentially included in the low- (20 MBq), medium- (40 MBq), and high-dose (60 MBq) groups. Positron emission tomography (PET)/CT imaging was used to check the occurrence of particle displacement postoperatively. After euthanasia, the pancreas and adjacent organs were excised for histological examination and residue radiation detection. The absorbed doses demonstrated safe in the porcine model were further in the xenograft model and <i>KRAS^LSL/+Trp53^FL/FLPtfqa^Cre/+</i> mouse model. EUS-guided implantations of ⁹⁰Y-loaded microspheres were successful in all animals. Two pigs had mild serum amylase elevation in the high-dose group and the abnormal index returned to baseline without interventions. The volume of necrotic lesions ranged from 255.76 to 745.57 mm³. In KPC mouse model, PET/CT imaging demonstrated a significant decrease in maximum standardized uptake value (SUVmax) after ⁹⁰Y implantation. EUS-guided ⁹⁰Y-loaded carbon microsphere implantation could serve as a safe and feasible technique at ultrahigh dose for pancreatic cancer brachytherapy.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70117","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481463","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SIRT1 Alleviates Mitochondrial Fission and Necroptosis in Cerebral Ischemia/Reperfusion Injury via SIRT1–RIP1 Signaling Pathway","authors":"Xuan Wei,&nbsp;Hanjing Guo,&nbsp;Guangshan Huang,&nbsp;Haoyue Luo,&nbsp;Lipeng Gong,&nbsp;Pan Meng,&nbsp;Jiyong Liu,&nbsp;Wenli Zhang,&nbsp;Zhigang Mei","doi":"10.1002/mco2.70118","DOIUrl":"https://doi.org/10.1002/mco2.70118","url":null,"abstract":"<p>Programmed cell death, including necroptosis, plays a critical role in the pathogenesis of cerebral ischemia/reperfusion injury (CIRI). Silent information regulator 1 (SIRT1) has been identified as a potential therapeutic target for CIRI, yet its precise role in regulating necroptosis remains controversial. Furthermore, the potential interaction between SIRT1 and receptor-interacting protein kinase 1 (RIP1) in this context is not fully understood. <i>Sanpian</i> Decoction (SPD), a classical traditional herbal formula, was previously shown to enhance SIRT1 expression in our studies. Our findings demonstrated that, both in vivo and in vitro, CIRI was associated with a decrease in SIRT1 levels and phosphorylated dynamin-related protein 1 (p-DRP1) at Ser637, alongside an increase in RIP1 and other necroptosis-related proteins. Co-immunoprecipitation and immunofluorescence analyses revealed a weakened interaction between SIRT1 and RIP1. Furthermore, abnormal mitochondrial fission and dysfunction were mediated through the phosphoglycerate mutase 5–DRP1 pathway. Notably, SPD treatment improved neurological outcomes and reversed these pathological changes by enhancing the SIRT1–RIP1 interaction. In conclusion, this study suggests that SIRT1 is a promising therapeutic target for CIRI, capable of inhibiting necroptosis and mitigating mitochondrial fission via the SIRT1–RIP1 pathway. SPD exhibits therapeutic potential by activating SIRT1, thereby attenuating necroptosis and mitochondrial fission during CIRI.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143481464","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sepsis: the evolution of molecular pathogenesis concepts and clinical management","authors":"Zhongxue Feng,&nbsp;Lijun Wang,&nbsp;Jing Yang,&nbsp;Tingting Li,&nbsp;Xuelian Liao,&nbsp;Yan Kang,&nbsp;Fei Xiao,&nbsp;Wei Zhang","doi":"10.1002/mco2.70109","DOIUrl":"https://doi.org/10.1002/mco2.70109","url":null,"abstract":"<p>The mortality rate of sepsis is approximately 22.5%, accounting for 19.7% of the total global mortality. Since Lewis Thomas proposed in 1972 that “it is our response that makes the disease (sepsis)” rather than the invading microorganisms, numerous drugs have been developed to suppress the “overwhelming” inflammatory response, but none of them has achieved the desired effect. Continued failure has led investigators to question whether deaths in septic patients are indeed caused by uncontrolled inflammation. Here, we review the history of clinical trials based on evolving concepts of sepsis pathogenesis over the past half century, summarize the factors that led to the failure of these historical drugs and the prerequisites for the success of future drugs, and propose the basic principles of preclinical research to ensure successful clinical translation. The strategy of targeting inflammatory factors are like attempting to eliminate invaders by suppressing the host's armed forces, which is logically untenable. Sepsis may not be that complex; rather, sepsis may be the result of a failure to fight microbes when the force of an invading pathogen overwhelms our defenses. Thus, strengthening the body's defense forces instead of suppressing them may be the correct strategy to overcome sepsis.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70109","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143475337","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ferroptosis in Pulmonary Disease and Lung Cancer: Molecular Mechanisms, Crosstalk Regulation, and Therapeutic Strategies","authors":"Dandan Guo,&nbsp;Songhua Cai,&nbsp;Lvdan Deng,&nbsp;Wangting Xu,&nbsp;Sentao Fu,&nbsp;Yaling Lin,&nbsp;Tong Jiang,&nbsp;Qing Li,&nbsp;Zhijun Shen,&nbsp;Jian Zhang,&nbsp;Peng Luo,&nbsp;Bufu Tang,&nbsp;Ling Wang","doi":"10.1002/mco2.70116","DOIUrl":"https://doi.org/10.1002/mco2.70116","url":null,"abstract":"<p>Ferroptosis is a distinct form of iron-dependent programmed cell death characterized primarily by intracellular iron accumulation and lipid peroxidation. Multiple cellular processes, including amino acid metabolism, iron metabolism, lipid metabolism, various signaling pathways, and autophagy, have been demonstrated to influence the induction and progression of ferroptosis. Recent investigations have elucidated that ferroptosis plays a crucial role in the pathogenesis of various pulmonary disorders, including lung injury, chronic obstructive pulmonary disease, pulmonary fibrosis, and asthma. Ferroptosis is increasingly recognized as a promising novel strategy for cancer treatment. Various immune cells within the tumor microenvironment, including CD8+ T cells, macrophages, regulatory T cells, natural killer cells, and dendritic cells, have been shown to induce ferroptosis in tumor cells and modulate the process through the regulation of iron and lipid metabolism pathways. Conversely, ferroptosis can reciprocally alter the metabolic environment, leading to the activation or inhibition of immune cell functions, thereby modulating immune responses. This paper reviews the molecular mechanism of ferroptosis and describes the tumor immune microenvironment, discusses the connection between ferroptosis and the tumor microenvironment in lung cancer and pulmonary diseases, and discusses the development prospect of their interaction in the treatment of lung cancer and pulmonary diseases.</p>","PeriodicalId":94133,"journal":{"name":"MedComm","volume":"6 3","pages":""},"PeriodicalIF":10.7,"publicationDate":"2025-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mco2.70116","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143475336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}