Frontiers in cell death最新文献

Sacrificing cells of the cyst: non-apoptotic cell death in germline cysts via acidification. 牺牲囊肿细胞：种系囊肿非凋亡细胞通过酸化死亡。

Frontiers in cell death Pub Date : 2025-01-01 Epub Date: 2025-10-28 DOI: 10.3389/fceld.2025.1677498

Shruthi Bandyadka, Logan Tohline, Georgette-Vanelle Wandji, Hila Toledano, Kimberly McCall

{"title":"Sacrificing cells of the cyst: non-apoptotic cell death in germline cysts via acidification.","authors":"Shruthi Bandyadka, Logan Tohline, Georgette-Vanelle Wandji, Hila Toledano, Kimberly McCall","doi":"10.3389/fceld.2025.1677498","DOIUrl":"10.3389/fceld.2025.1677498","url":null,"abstract":"Cell death shapes multicellular organism development and sustains tissue and organ homeostasis. Great progress has been made in understanding the breadth of physiological and biochemical diversity in cell death and clearance pathways, which play vital roles in organismal development and health. While apoptosis and necrosis have been studied extensively across many model systems and contexts, the discovery of non-apoptotic paradigms of cell death and their roles in disease has greatly expanded the field. Collectively called Regulated Cell Death, these death pathways operate in a tissue and context-dependent manner. Germ cells in many organisms develop in cysts of interconnected cells, and may die in response to environmental or developmental cues. Recent findings suggest that germ cell cysts may use a common mechanism of non-apoptotic cell death involving phagocytic and lysosomal activity of surrounding somatic cells. Cyst cell death has been analyzed most thoroughly in the Drosophila adult ovary and testis, with remarkable similarity to cyst cell death in mouse adult testis and fetal ovary. In this review, we highlight recent progress in deciphering germline cyst cell death.","PeriodicalId":73072,"journal":{"name":"Frontiers in cell death","volume":"4 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12716865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145806671","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}

引用次数: 0

C/EBPβ Deficiency Enhances Keratinocyte Apoptosis after UVB-Induced DNA Damage via Regulation of the Type I IFN and TNF Responses. C/EBPβ缺乏通过调节I型IFN和TNF反应增强uvb诱导的DNA损伤后角质细胞凋亡

Frontiers in cell death Pub Date : 2025-01-01 Epub Date: 2025-09-02 DOI: 10.3389/fceld.2025.1658598

Emma E Tobin, Ayushma Sharma, Samantha T Kros, Dereje D Jima, Sophia C Gray, Jonathan R Hall

{"title":"C/EBPβ Deficiency Enhances Keratinocyte Apoptosis after UVB-Induced DNA Damage via Regulation of the Type I IFN and TNF Responses.","authors":"Emma E Tobin, Ayushma Sharma, Samantha T Kros, Dereje D Jima, Sophia C Gray, Jonathan R Hall","doi":"10.3389/fceld.2025.1658598","DOIUrl":"10.3389/fceld.2025.1658598","url":null,"abstract":"The epidermis is routinely subjected to DNA damage induced by ultraviolet B (UVB) solar radiation. In addition to activating canonical DNA damage responses such as cycle cell checkpoints and DNA repair, UVB-induced DNA damage can also activate additional signaling pathways including inflammatory responses. The pathways activated downstream of UVB-induced DNA damage have a critical role in determining cellular survival to UVB radiation. Here we report that loss of CCAAT/enhancer binding protein β (C/EBPβ) in mouse keratinocytes results in enhanced UVB-induced apoptosis through activation of extrinsic apoptosis genes cleaved caspase-8 and truncated BH3 interacting-domain death agonist (tBid). RNAseq and Ingenuity Pathway Analysis of UVB-treated C/EBPβ-/- primary keratinocytes revealed an enrichment of inflammatory signaling pathways, including the type I interferon (IFN-I) pathway as the most enriched pathway. Numerous IFN-I stimulated genes were up-regulated in UVB-treated C/EBPβ-/- keratinocytes, including genes that regulate extrinsic apoptosis. Inhibition of the interferon α/β receptor or the associated kinase Tyk2 greatly reduced cell death in UVB-exposed C/EBPβ deficient keratinocytes, demonstrating the dependence of IFN signaling in C/EBPβ regulated apoptosis. The apoptosis inducing cytokine tumor necrosis factor alpha (TNF-α) was identified as one of the most significant upstream regulators activated in UVB-exposed C/EBPβ-/- keratinocytes compared to UVB exposed wild type control. UVB-exposed C/EBPβ-/- keratinocytes displayed increased expression of TNF-α and the enhanced apoptosis in C/EBPβ-/- keratinocytes was suppressed by a TNF-α neutralizing antibody. Our results indicate that loss of C/EBPβ enhances activation of a non-canonical UVB DNA damage response pathway involving interferon and TNF signaling to induce keratinocyte cell death.","PeriodicalId":73072,"journal":{"name":"Frontiers in cell death","volume":"4 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13007985/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147517278","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}

引用次数: 0

Exploring Sugar-Induced Cell Death (SICD) in Yeast: Implications for Diabetes and Cancer Research. 酵母中糖诱导的细胞死亡（SICD）：对糖尿病和癌症研究的意义。

Frontiers in cell death Pub Date : 2025-01-01 Epub Date: 2025-03-18 DOI: 10.3389/fceld.2025.1470093

Raveena Parbhudayal, Hai-Ping Cheng

{"title":"Exploring Sugar-Induced Cell Death (SICD) in Yeast: Implications for Diabetes and Cancer Research.","authors":"Raveena Parbhudayal, Hai-Ping Cheng","doi":"10.3389/fceld.2025.1470093","DOIUrl":"10.3389/fceld.2025.1470093","url":null,"abstract":"When yeast cells are transferred to water only, they remain viable for several days. However, when transferred to water with glucose, there is a rapid loss of viability. This phenomenon is termed Sugar-Induced Cell Death (SICD). In addition to glucose, SICD can be induced by an array of different sugars and is thought to be triggered by increased levels of intracellular reactive oxygen species (ROS) generated upon transfer to sugar-only solutions. Although not termed SICD, a similar response is observed in mammalian cells, whereby high glucose induces cell death, especially in cases of hyperglycemia and diabetes. In contrast, cancer cells thrive under conditions of high glucose. In this review, we summarize the current understanding of SICD in yeast and highlight studies showing the presence of a similar phenomenon in mammalian cells, High Glucose-Induced Cell Death (HGICD). We end with a discussion on mechanisms by which cancer cells evade HGICD. Unlike other types of cell death in yeast, SICD has not yet been thoroughly reviewed. Therefore, this review represents the first comprehensive review of SICD in yeast with a comparison to HGICD in other eukaryotes.","PeriodicalId":73072,"journal":{"name":"Frontiers in cell death","volume":"4 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12539669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145350200","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}

引用次数: 0

ATF4-mediated expression of NOXA is critical for Necroptosis driven by Glucose Deprivation. atf4介导的NOXA表达对葡萄糖剥夺引起的坏死性下垂至关重要。

Frontiers in cell death Pub Date : 2025-01-01 Epub Date: 2025-01-20 DOI: 10.3389/fceld.2024.1507960

Sasiprapa Sonkaew, Ruwaida Rajna, Yeon-Ji Park, Jiong Yan, Zhaoshan Liu, Siriporn Jitkaew, Zheng-Gang Liu, Swati Choksi

引用次数: 0

The sea urchin embryo and the cell stress responses: new perspectives 海胆胚胎和细胞应激反应：新视角

Frontiers in cell death Pub Date : 2024-07-23 DOI: 10.3389/fceld.2024.1422224

I. Deidda, R. Russo, Nadia Lampiasi, F. Zito, R. Bonaventura

{"title":"The sea urchin embryo and the cell stress responses: new perspectives","authors":"I. Deidda, R. Russo, Nadia Lampiasi, F. Zito, R. Bonaventura","doi":"10.3389/fceld.2024.1422224","DOIUrl":"https://doi.org/10.3389/fceld.2024.1422224","url":null,"abstract":"In addition to many industrial activities that release pollutants in coastal areas, numerous human behaviors contribute to climate change, inducing global warming, which can also reshape the environmental impacts of some pollutants. Therefore, it is extremely important to develop new tools that can detect pollutants and environmental changes quickly and easily with high levels of sensitivity. The sea urchin embryo is a well-known model used worldwide in many research fields, including marine ecotoxicology, as a huge range of contaminants can affect its embryonic development with species-specific sensitivity. Morphological abnormalities are already considered biomarkers to evaluate the effects of pollutants, and, indeed, the sea urchin has long been used as one of the key species in a battery of bioassays to assess the toxicity of many pollutants and dredged sediments. At the cellular level, the molecular mechanisms activated against a stress agent constitute what is known as the “cell stress response,” analyzed here within a whole organism, namely, the sea urchin embryo. In this minireview, we have reported the available molecular biomarkers linked to morphological abnormalities and the genes affected by environmental changes and emerging pollutants, highlighting those studies that use high-throughput screening approaches to evaluate the effects of environmental conditions on sea urchin embryos.","PeriodicalId":73072,"journal":{"name":"Frontiers in cell death","volume":"26 9","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141813661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Non-canonical functions of regulated cell death machinery regulate cellular growth, invasion and the interplay between cell death modalities 细胞死亡调控机制的非规范功能可调控细胞生长、入侵以及细胞死亡模式之间的相互作用

Frontiers in cell death Pub Date : 2024-07-15 DOI: 10.3389/fceld.2024.1423805

Y. Shan, B. Mollereau

引用次数: 0

Regulatory signaling pathways of osteoblast autophagy in periprosthetic osteolysis 假体周围溶骨过程中成骨细胞自噬的调控信号通路

Frontiers in cell death Pub Date : 2024-02-05 DOI: 10.3389/fceld.2024.1337724

YingChu Gu, ZeRui Wu, Heng Xie, Tao Fang, Qiufei Wang, Ye Gu

{"title":"Regulatory signaling pathways of osteoblast autophagy in periprosthetic osteolysis","authors":"YingChu Gu, ZeRui Wu, Heng Xie, Tao Fang, Qiufei Wang, Ye Gu","doi":"10.3389/fceld.2024.1337724","DOIUrl":"https://doi.org/10.3389/fceld.2024.1337724","url":null,"abstract":"Periprosthetic osteolysis is a difficult-to-treat complication of arthroplasty. The pathological mechanisms of periprosthetic osteolysis are mainly weakened function of osteoblasts and excessive activation of osteoclasts. Many studies have demonstrated that the imbalance between the formation of bone by osteoblasts and the absorption of bone by osteoclasts is the direct cause of osteolytic diseases. Autophagy, as an important self-protective cellular mechanism, has significant effects on the regulation of osteoblast function, such as osteoblast differentiation, proliferation, and apoptosis. Osteoblasts, which play an important role in maintaining bone homeostasis, have attracted increasing attention in recent years. Up till now, Several signaling pathways have been proved to regulate autophagy of osteoblasts, including the AMPK, NF-κB, FoxO3 and other signaling pathways. This article reviews the recent progress in understanding osteoblast autophagy and mitophagy in the context of periprosthetic osteolysis and the signaling pathways which are involved in these processes. By summarizing previous studies describing the mechanism underlying osteoblast autophagy, we wish to contribute new therapeutic ideas and potential therapeutic targets for periprosthetic osteolysis.","PeriodicalId":73072,"journal":{"name":"Frontiers in cell death","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139864238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Regulatory signaling pathways of osteoblast autophagy in periprosthetic osteolysis 假体周围溶骨过程中成骨细胞自噬的调控信号通路

Frontiers in cell death Pub Date : 2024-02-05 DOI: 10.3389/fceld.2024.1337724

YingChu Gu, ZeRui Wu, Heng Xie, Tao Fang, Qiufei Wang, Ye Gu

{"title":"Regulatory signaling pathways of osteoblast autophagy in periprosthetic osteolysis","authors":"YingChu Gu, ZeRui Wu, Heng Xie, Tao Fang, Qiufei Wang, Ye Gu","doi":"10.3389/fceld.2024.1337724","DOIUrl":"https://doi.org/10.3389/fceld.2024.1337724","url":null,"abstract":"Periprosthetic osteolysis is a difficult-to-treat complication of arthroplasty. The pathological mechanisms of periprosthetic osteolysis are mainly weakened function of osteoblasts and excessive activation of osteoclasts. Many studies have demonstrated that the imbalance between the formation of bone by osteoblasts and the absorption of bone by osteoclasts is the direct cause of osteolytic diseases. Autophagy, as an important self-protective cellular mechanism, has significant effects on the regulation of osteoblast function, such as osteoblast differentiation, proliferation, and apoptosis. Osteoblasts, which play an important role in maintaining bone homeostasis, have attracted increasing attention in recent years. Up till now, Several signaling pathways have been proved to regulate autophagy of osteoblasts, including the AMPK, NF-κB, FoxO3 and other signaling pathways. This article reviews the recent progress in understanding osteoblast autophagy and mitophagy in the context of periprosthetic osteolysis and the signaling pathways which are involved in these processes. By summarizing previous studies describing the mechanism underlying osteoblast autophagy, we wish to contribute new therapeutic ideas and potential therapeutic targets for periprosthetic osteolysis.","PeriodicalId":73072,"journal":{"name":"Frontiers in cell death","volume":"72 3","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139804576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Die Hard: Necroptosis and its Impact on Age-Dependent Neuroinflammatory Diseases. 虎胆龙威：坏死性下垂及其对年龄依赖性神经炎性疾病的影响。

Frontiers in cell death Pub Date : 2024-01-01 Epub Date: 2024-03-08 DOI: 10.3389/fceld.2024.1348153

Kaitlan Smith, Meagan Colie, Trinity Moore, Jonathan C Schisler

{"title":"Die Hard: Necroptosis and its Impact on Age-Dependent Neuroinflammatory Diseases.","authors":"Kaitlan Smith, Meagan Colie, Trinity Moore, Jonathan C Schisler","doi":"10.3389/fceld.2024.1348153","DOIUrl":"10.3389/fceld.2024.1348153","url":null,"abstract":"The pro-inflammatory form of cellular death, necroptosis, is critical to age-related pathologies. Necroptosis primarily functions as an antipathogenic and antitumor biological mechanism by triggering inflammatory pathways within rogue cell bodies, resulting in cell death. Several neurodegenerative conditions have hallmarks of necroptosis, suggesting a potential role for this cell death pathway in the pathogenesis of neuroinflammation and neuronal cell death, likely through the release of pro-inflammatory cytokines that perpetuate inflammatory signaling and neurodegeneration. The receptor-interacting protein kinases 1 and 3 (RIPK1/3) signaling cascade is critical to necroptosis regulation; however, the complete mechanism behind necroptotic activation, regulation, and resolution remains incomplete. In cases where necroptosis is disadvantageous, such as neurodegenerative diseases, we lack effective pharmacological suppressors of necroptosis that could mitigate disease progression. Targeting regulatory proteins within the necroptotic signaling pathway has shown promise; however, the need for specific inhibitors limits therapeutic opportunities. This review focuses on necroptosis and its role in neuroinflammation and neurodegeneration in age-dependent disorders. We comprehensively detail the known necroptotic signaling pathways and potential signaling partners and discuss the ongoing therapeutic efforts in targeting and preventing active necroptotic signaling and their relevance to neuroprotection.","PeriodicalId":73072,"journal":{"name":"Frontiers in cell death","volume":"3 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12309338/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144755259","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}

引用次数: 0

The histone demethylase Kdm5 controls Hid-induced cell death in Drosophila. 组蛋白去甲基化酶Kdm5控制hid诱导的果蝇细胞死亡。

Frontiers in cell death Pub Date : 2024-01-01 Epub Date: 2024-11-19 DOI: 10.3389/fceld.2024.1471050

Hans-Martin Herz, Andreas Bergmann

{"title":"The histone demethylase Kdm5 controls Hid-induced cell death in Drosophila.","authors":"Hans-Martin Herz, Andreas Bergmann","doi":"10.3389/fceld.2024.1471050","DOIUrl":"10.3389/fceld.2024.1471050","url":null,"abstract":"We conducted an EMS mutagenesis screen on chromosome arm 2L to identify recessive suppressors of GMR-hid-induced apoptosis in the Drosophila eye. Through this screen, we recovered three alleles of the lysine demethylase gene Kdm5. Kdm5, a member of the JmjC-domain-containing protein family, possesses histone demethylase activity towards H3K4me3. Our data suggest that Kdm5 specifically regulates Hid-induced cell death during development, as we did not observe control of Reaper- or Grim-induced cell death by Kdm5. Interestingly, GMR-hid-induced apoptosis is suppressed independently of Kdm5's demethylase activity. Our findings indicate that Rbf and dMyc are necessary for Kdm5 mosaics to suppress GMR-hid-induced cell death. Moreover, Kdm5 mosaics failed to suppress apoptosis induced by a mutant form of Hid that is resistant to inhibition by Erk-type MAPK activity. Additionally, Kdm5 dominantly enhances the wing phenotype of an activated MAPK mutant. These results collectively suggest that Kdm5 controls Hid-induced apoptosis by regulating the Rbf, dMyc, and MAPK pathways.","PeriodicalId":73072,"journal":{"name":"Frontiers in cell death","volume":"3 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101616/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144144906","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}

引用次数: 0