Ferroptosis, necroptosis, pyroptosis, and cuproptosis in cancer: a comparative bibliometric analysis.
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ABSTRACT:
SUBMITTER: Wu H
PROVIDER: S-EPMC10333212 | biostudies-literature | 2023 Jul
REPOSITORIES: biostudies-literature
Publications
Ferroptosis, necroptosis, pyroptosis, and cuproptosis in cancer: a comparative bibliometric analysis.
Wu Haiyang H Cheng Kunming K Li Cheng C
Cell death discovery 20230710 1
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Project description:This study aims to visualize research hotspots and trends of "ferroptosis in cancer", "necroptosis in cancer", "pyroptosis in cancer", and "cuproptosis in cancer" through a bibliometric analysis to facilitate understanding of future developments in basic and clinical research and to provide a new perspective on cancer treatment. From January 1, 2012 to October 31, 2022, in the field of "ferroptosis in cancer", a total of 2467 organizations from 79 different countries published 3302 articles. 2274 organizations from 72 different countries published 2233 articles in the field of " necroptosis in cancer". 1366 institutions from 58 different countries contributed 1445 publications in the field of "pyroptosis in cancer". In the field of " cuproptosis in cancer", the number of articles published in the last 10 years is relatively low, with a total of 109 articles published by 116 institutions from four different countries. In the field of "ferroptosis in cancer", Tang Daolin had published 66 documents, ranked the first, while Dixon SJ is the most cited author, cited 3148 times; In the fields of "necroptosis in cancer", Vandenabeele peter had published 35 papers and Degterev had been cited 995 times, ranked the first, respectively; Kanneganti thirumala-devi had published 24 papers, is the highest number of publications in the fields of "pyroptosis in cancer", while Shi JJ was the most cited author with being cited 508 times. Both Huang Yan and Wang Tao published three papers and tied for first place and Tsvetkov p ranks first with being cited 107 times in "cuproptosis in cancer". "Cell", "Cell", "Nature", and "Science" was the most frequently co-cited journal on "ferroptosis in cancer", "necroptosis in cancer", "pyroptosis in cancer", and "cuproptosis in cancer", respectively. Further exploration of inhibitors of different Programmed cell death (PCD) and their targeted therapies are potential treatment options for cancer, but more direct clinical evidence as well as higher level clinical trials remain to be explored. Further clarification of the mechanisms of crosstalk between these PCDs may provide effective cancer treatments. And the role of different types of PCDs, especially the novel ones discovered, in cancer can be expected to remain a hot topic of research in the cancer field for quite some time to come.
| S-EPMC10105750 | biostudies-literature
Project description:Many types of human cells self-destruct to maintain biological homeostasis and defend the body against pathogenic substances. This process, called regulated cell death (RCD), is important for various biological activities, including the clearance of aberrant cells. Thus, RCD pathways represented by apoptosis have increased in importance as a target for the development of cancer medications in recent years. However, because tumor cells show avoidance to apoptosis, which causes treatment resistance and recurrence, numerous studies have been devoted to alternative cancer cell mortality processes, namely necroptosis, pyroptosis, ferroptosis, and cuproptosis; these RCD modalities have been extensively studied and shown to be crucial to cancer therapy effectiveness. Furthermore, evidence suggests that tumor cells undergoing regulated death may alter the immunogenicity of the tumor microenvironment (TME) to some extent, rendering it more suitable for inhibiting cancer progression and metastasis. In addition, other types of cells and components in the TME undergo the abovementioned forms of death and induce immune attacks on tumor cells, resulting in enhanced antitumor responses. Hence, this review discusses the molecular processes and features of necroptosis, pyroptosis, ferroptosis, and cuproptosis and the effects of these novel RCD modalities on tumor cell proliferation and cancer metastasis. Importantly, it introduces the complex effects of novel forms of tumor cell death on the TME and the regulated death of other cells in the TME that affect tumor biology. It also summarizes the potential agents and nanoparticles that induce or inhibit novel RCD pathways and their therapeutic effects on cancer based on evidence from in vivo and in vitro studies and reports clinical trials in which RCD inducers have been evaluated as treatments for cancer patients. Lastly, we also summarized the impact of modulating the RCD processes on cancer drug resistance and the advantages of adding RCD modulators to cancer treatment over conventional treatments.
| S-EPMC9733270 | biostudies-literature
Project description:In recent years, cancer immunotherapy based on immune checkpoint inhibitors (ICIs) has achieved considerable success in the clinic. However, ICIs are significantly limited by the fact that only one third of patients with most types of cancer respond to these agents. The induction of cell death mechanisms other than apoptosis has gradually emerged as a new cancer treatment strategy because most tumors harbor innate resistance to apoptosis. However, to date, the possibility of combining these two modalities has not been discussed systematically. Recently, a few studies revealed crosstalk between distinct cell death mechanisms and antitumor immunity. The induction of pyroptosis, ferroptosis, and necroptosis combined with ICIs showed synergistically enhanced antitumor activity, even in ICI-resistant tumors. Immunotherapy-activated CD8+ T cells are traditionally believed to induce tumor cell death via the following two main pathways: (i) perforin-granzyme and (ii) Fas-FasL. However, recent studies identified a new mechanism by which CD8+ T cells suppress tumor growth by inducing ferroptosis and pyroptosis, which provoked a review of the relationship between tumor cell death mechanisms and immune system activation. Hence, in this review, we summarize knowledge of the reciprocal interaction between antitumor immunity and distinct cell death mechanisms, particularly necroptosis, ferroptosis, and pyroptosis, which are the three potentially novel mechanisms of immunogenic cell death. Because most evidence is derived from studies using animal and cell models, we also reviewed related bioinformatics data available for human tissues in public databases, which partially confirmed the presence of interactions between tumor cell death and the activation of antitumor immunity.
| S-EPMC7418434 | biostudies-literature
Project description:In recent years, immunotherapy represented by immune checkpoint inhibitors (ICIs) has led to unprecedented breakthroughs in cancer treatment. However, the fact that many tumors respond poorly or even not to ICIs, partly caused by the absence of tumor-infiltrating lymphocytes (TILs), significantly limits the application of ICIs. Converting these immune "cold" tumors into "hot" tumors that may respond to ICIs is an unsolved question in cancer immunotherapy. Since it is a general characteristic of cancers to resist apoptosis, induction of non-apoptotic regulated cell death (RCD) is emerging as a new cancer treatment strategy. Recently, several studies have revealed the interaction between non-apoptotic RCD and antitumor immunity. Specifically, autophagy, ferroptosis, pyroptosis, and necroptosis exhibit synergistic antitumor immune responses while possibly exerting inhibitory effects on antitumor immune responses. Thus, targeted therapies (inducers or inhibitors) against autophagy, ferroptosis, pyroptosis, and necroptosis in combination with immunotherapy may exert potent antitumor activity, even in tumors resistant to ICIs. This review summarizes the multilevel relationship between antitumor immunity and non-apoptotic RCD, including autophagy, ferroptosis, pyroptosis, and necroptosis, and the potential targeting application of non-apoptotic RCD to improve the efficacy of immunotherapy in malignancy.
| S-EPMC9208265 | biostudies-literature
Project description:BackgroundAlzheimer's disease (AD) is a genetically intricate neurodegenerative disorder. Studies on "Ferroptosis in AD", "Pyroptosis in AD", and "Necroptosis in AD" are becoming more prevalent and there is increasing evidence that they are closely related to AD. However, there has not yet been a thorough bibliometrics-based investigation on this subject.ObjectiveThis study uses a bibliometric approach to visualize and analyze the literature within the field of three distinct types of cell death in AD and explores the current research hotspots and prospective research directions.MethodsWe collected relevant articles from the Web of Science and used CiteSpace, VOS viewer, and Pajek to perform a visual analysis.ResultsA total of 123, 95, and 84 articles were published in "Ferroptosis in AD", "Pyroptosis in AD", and "Necroptosis in AD", respectively. Based on keywords analysis, we can observe that "oxidative stress" and "lipid peroxidation", "cell death" and "activation", and "Nlrp3 inflammasome" and "activation" were the three most prominent words in the field of "Ferroptosis in AD", "Pyroptosis in AD", and "Necroptosis in AD", respectively. Focusing on the breakout words in the keyword analysis, we reviewed the mechanisms of ferroptosis, pyroptosis, and necroptosis in AD. By mapping the time zones of the keywords, we speculated on the evolutionary trends of ferroptosis, pyrotosis, and necroptosis in AD.ConclusionsOur findings can help researchers grasp the research status of three types of cell death in AD and determine new directions for future research as soon as possible.
| S-EPMC10836606 | biostudies-literature
Project description:Bronchial asthma is a complex heterogeneous airway disease, which has emerged as a global health issue. A comprehensive understanding of the different molecular mechanisms of bronchial asthma may be an efficient means to improve its clinical efficacy in the future. Increasing research evidence indicates that some types of programmed cell death (PCD), including apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis, contributed to asthma pathogenesis, and may become new targets for future asthma treatment. This review briefly discusses the molecular mechanism and signaling pathway of these forms of PCD focuses on summarizing their roles in the pathogenesis and treatment strategies of asthma and offers some efficient means to improve clinical efficacy of therapeutics for asthma in the near future.
| S-EPMC10321329 | biostudies-literature
Project description:Radiotherapy (RT) stands as the primary treatment for tumors, but it inevitably causes damage to normal cells. Consequently, radiation injury is a crucial consideration for radiation oncologists during therapy planning. Cell death including apoptosis, autophagy, pyroptosis, ferroptosis, and necroptosis play significant roles in tumor treatment. While previous studies elucidated the induction of apoptosis and autophagy by ionizing radiation (IR), recent attention has shifted to pyroptosis, ferroptosis, and necroptosis, revealing their effects induced by IR. This review aims to summarize the strategies employed by IR, either alone or in combination therapy, to induce pyroptosis, ferroptosis, and necroptosis in radiation injury. Furthermore, we explore their effects and molecular pathways, shedding light on their roles in radiation injury. Finally, we summarize the regulative agents for these three types of cell death and their mechanisms. In summary, optimizing radiation dose, dose rate, and combined treatment plans to minimize radiation damage and enhance the killing effect of RT is a key focus.
| S-EPMC10929204 | biostudies-literature
Project description:Introduction: Periodontitis is a chronic inflammatory oral disease that destroys soft and hard periodontal support tissues. Multiple cell death modes including apoptosis, necroptosis, pyroptosis, and ferroptosis play a crucial role in the pathogenicity of inflammatory diseases. This study aimed to identify genes associated with ferroptosis, necroptosis, and pyroptosis in different cells present in the periodontium of periodontitis patients. Methods: Gingival tissues' mRNA sequencing dataset GSE173078 of 12 healthy control and 12 periodontitis patients' and the microarray dataset GSE10334 of 63 healthy controls and 64 periodontitis patients' were obtained from Gene Expression Omnibus (GEO) database. A total of 910 differentially expressed genes (DEGs) obtained in GSE173078 were intersected with necroptosis, pyroptosis, and ferroptosis-related genes to obtain the differential genes associated with cell death (DCDEGs), and the expression levels of 21 differential genes associated with cell death were verified with dataset GSE10334. Results: Bioinformatic analysis revealed 21 differential genes associated with cell death attributed to ferroptosis, pyroptosis, and necroptosis in periodontitis patients compared with healthy controls. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses revealed that 21 differential genes associated with cell death were related to various cellular and immunological pathways including inflammatory responses, necroptosis, and osteoclast differentiation. Additionally, the single-cell RNA (scRNA) sequencing data GSE171213 of 4 healthy controls and 5 periodontitis patients' periodontal tissue was analyzed to obtain cell clustering and cell types attributed to differential genes associated with cell death. We found that among 21 DCDEGs, SLC2A3, FPR2, TREM1, and IL1B were mainly upregulated in neutrophils present in the periodontium of periodontitis patients. Gene overlapping analysis revealed that IL-1B is related to necroptosis and pyroptosis, TREM1 and FPR2 are related to pyroptosis, and SLC2A3 is related to ferroptosis. Finally, we utilized the CIBERSORT algorithm to assess the association between DCDEGs and immune infiltration phenotypes, based on the gene expression profile of GSE10334. The results revealed that the upregulated SLC2A3, FPR2, TREM1, and IL1B were positively correlated with neutrophil infiltration in the periodontium. Discussion: The findings provide upregulated SLC2A3, FPR2, TREM1, and IL1B in neutrophils as a future research direction on the mode and mechanism of cell death in periodontitis and their role in disease pathogenicity.
| S-EPMC9852864 | biostudies-literature
Project description:Background: Ferroptosis is a novel mechanism of programmed cell death coined in 2012, which has been found to play important roles in human health and disease. In the past decade, ferroptosis research has seen booming growth worldwide. The aim of this study was to visualize the scientific outputs and research trends of ferroptosis in the field of cancer. Methods: The raw data of publications were retrieved from the Web of Science Core Collection on 19 December 2021. The information on the impact factor (IF) and Journal Citation Reports (JCR) division were obtained from the website of Web of Science. Two kinds of software (CiteSpace and VOSviewer) were used to perform visualized analysis. Results: From 2012 to 2021, a total of 1833 publications related to ferroptosis in cancer were identified for final analysis. The annual number of citations and publications grew exponentially over the past decade. China (1,092) and United States (489) had the highest number of publications; Central South University and Guangzhou Medical University were the most productive institutions. Daolin Tang and Scott J Dixon were the most active authors ranked by most productive and co-cited, respectively. The journals with the highest output and co-citation frequency were Biochemical and Biophysical Research Communications and Cell, respectively. Among the 1833 publications, four were identified with citations more than 1000 times. Six co-cited references had a citation burst duration until 2021. Analysis of keywords suggested the current research of ferroptosis in cancer clusters in 9 hotspots and newly emerging frontier may be "multidrug resistance". Conclusion: Cancer research is the major area of active research in ferroptosis. Our results provide a global landscape of the ferroptosis research in cancer from 2012 to 2021, which serves as a reference for future studies in this field.
| S-EPMC9174675 | biostudies-literature
Project description:The formation of extracellular vesicles (EVs) has emerged as a novel paradigm in cell-to-cell communication during health and disease. According to the type of cell death modalities, the intercellular functions of EVs may be influenced by their biogenesis and composition. To identify a possible EV cargo signature, we performed a comparative analysis of steady-state (ssEVs) and cell death-associated EVs (cdEVs) following apoptosis (apoEVs), necroptosis (necEVs) and ferroptosis (ferEVs) in the same cell type. We determined the physical and biochemical characteristics, the protein cargo by mass spectrometry.
2023-10-12 | PXD039297 | Pride