Different Types Of Cell Death Research Articles

Iron Metabolism and Ferroptosis in Early Brain Injury after Subarachnoid Haemorrhage.

At present, it appears that the prognosis for subarachnoid haemorrhage (SAH), which has a high death and disability rate, cannot be greatly improved by medication or other treatment. Recent research suggests that different types of cell death are implicated in early brain injury (EBI) after SAH, and this has been recognised as a major factor impacting the prognosis of SAH. Ferroptosis, which is a recently identified imbalance of iron metabolism and programmed cell death triggered by phospholipid peroxidation, has been shown to be involved in EBI after SAH and is thought to have a significant impact on EBI. The decomposition of cleaved haemoglobin during SAH involves the release of enormous amounts of free iron, resulting in iron metabolism disorders. Potential therapeutic targets for the signalling pathways of iron metabolism disorders and ferroptosis after SAH are constantly being discovered. To serve as a guide for research into other possible therapeutic targets, this paper will briefly describe the mechanisms of dysregulated iron metabolism and ferroptosis in the pathogenesis of SAH and highlight how they are involved in the development and promotion of EBI in SAH.

Bryonia aspera Root Extracts Induce Programmed Cell Death in Selected Cell Lines of Glioblastoma, Ovarian, and Breast Cancer

Background. Medicinal plants have been remarkable sources of current chemotherapeutic agents. Ethnobotanical utilization of Bryonia species goes back to the old era, and contemporary but preliminary studies have evidenced the anticancer effects of this kind of plant. Methods. The MTT assay was used to investigate the cytotoxicity of a range of concentrations from different extracts of Bryonia aspera root in cancer and noncancer cells. The apoptosis was assessed using annexinV-FITC/PI flow cytometry assay. The expression of selected hallmark genes from different cell death modalities, including apoptosis, necroptosis, ferroptosis, and pyroptosis, was investigated using the qPCR method. The ROS production was also measured by the fluorescence technique. Results. Compared to the normal cells, all three extracts could induce significant cell death in lower doses in breast, ovarian, and glioblastoma cancer cells. Flow cytometry and gene expression studies revealed that different extracts of Bryonia aspera tend to induce different types of cell death in the selective cancer cell lines. ROS production was not impacted significantly by any of those three extracts in none of the cancer cells. Conclusion. The findings showed that all three extracts of Bryonia aspera root contain biologically active compounds that induce different types of programmed cell death in the investigated breast, ovarian, and glioblastoma cancer cells in concentrations significantly less than the doses affecting normal cells.

Design and Synthesis of Aspirin-chalcone Mimic Conjugates as Potential Anticancer Agents.

Extensive research has been conducted on aspirin, a widely recognized NSAID medication, regarding its potential as an anticancer agent. Studies have revealed its ability to trigger cell death in different types of cancer cells. A set of aspirin-chalcone mimic conjugates 5a-k and 6a-d utilizing the freshly prepared acid chloride of aspirin moiety has been designed and synthesized. To evaluate the newly developed compounds, the NCI 60- cell line panel was employed to assess their anti-proliferative properties. Subsequently, cell cycle analysis was conducted along with an examination of the compounds' impact on the levels of p53, Bax, Bcl-2, active caspase- 3, and their inhibition mechanism of tubulin polymerization. Derivative 6c displayed the best anticancer activity among the tested series while 6d was the best against breast cancer MDA-MB-468, therefore both of them were selected for the 5-dose stage, however, targeting MDA-MB-468, PI-flow cytometry of compound 6d proved the triggered cell growth arrest at the G1/S phase avoiding the mitotic cycle in MDA-MB-468 cells. Similarly, the upregulation of oncogenic parameters such as caspase-3, p53, and Bax/Bcl-2, along with the inhibition of PARP-1 enzyme level, was observed with compound 6d. This compound also exhibited a significant ability to induce apoptosis and disrupt the intracellular microtubule network through a promising activity as a tubulin polymerization inhibitor with IC50 = 1.065 ± 0.024 ng/ml. Furthermore, to examine the manner in which compound 6d binds to the active pocket of the tubulin polymerization enzyme, a molecular docking study was conducted. The study indicated that compound 6d could be a powerful microtubule-destabilizing agent. Therefore, further research on 6d could be worthwhile.

Prognostic value of different radiation-related cell death genes in patients with lung adenocarcinoma

Background and aimsRadiotherapy is widely applied for lung adenocarcinoma (LUAD), while individualized differences led to different outcomes. This study aimed to establish a multi-gene risk scoring model to predict the benefits of LUAD patients from radiotherapy, based on different types of cell death respectively. ResultsOther than autophagy, pyroptosis, ferroptosis and Immunogenic cell death (ICD), the LUAD prognostic model based on apoptosis had the best performance, and the area under curves (AUCs) of the receiver operating curve (ROC) for 1-, 3-, and 5-year OS were 0.700,0.736,0.723,respectively. Such genes were involved as SLC7A5, EXO1, ABAT, NLRP1 and GAR1. Then patients were divided into high and low risk groups by the median apoptosis-LUAD risk score. For patients in the high-risk group, i.e., the radiotherapy-tolerant group, we screened adjuvant chemotherapy and found that besides the conventional first-line chemotherapy regimen, drugs such as Fludarabine, Pevonedistat, and Podophyllotoxin Bromide may also have potential therapeutic value. ConclusionThe multi-gene risk scoring model based on apoptosis might predict the radiotherapy benefits of LUAD patients and for those radioresistant patients classified by the model we also provided effective adjuvant chemicals, which would be used to guide clinical treatment.

Experimental evidence for Parthanatos-like mode of cell death of heat-damaged human skin fibroblasts in a cell culture-based in vitro burn model

The cellular mechanisms of burn conversion of heat damaged tissue are center of many studies. Even if the molecular mechanisms of heat-induced cell death are controversially discussed in the current literature, it is widely accepted that caspase-mediated apoptosis plays a central role. In the current study we wanted to develop further information on the nature of the mechanism of heat-induced cell death of fibroblasts in vitro. We found that heating of human fibroblast cultures (a 10 s rise from 37 °C to 67 °C followed by a 13 s cool down to 37 °C) resulted in the death of about 50% of the cells. However, the increase in cell death started with a delay, about one hour after exposure to heat, and reached the maximum after about five hours. The lack of clear evidence for an active involvement of effector caspase in the observed cell death mechanism and the lack of observation of the occurrence of hypodiploid nuclei contradict heat-induced cell death by caspase-mediated apoptosis. Moreover, a dominant heat-induced increase in PARP1 protein expression, which correlated with a time-delayed ATP synthesis inhibition, appearance of double-strand breaks and secondary necrosis, indicate a different type of cell death than apoptosis. Indeed, increased translocation of Apoptosis Inducing Factor (AIF) and Macrophage Migration Inhibitory Factor (MIF) into cell nuclei, which correlates with the mentioned enhanced PARP1 protein expression, indicate PARP1-induced, AIF-mediated and MIF-activated cell death. With regard to the molecular actors involved, the cellular processes and temporal sequences, the mode of cell death observed in our model is very similar to the cell death mechanism via Parthanatos described in the literature.

The mechanism by which piR-000699 targets SLC39A14 regulates ferroptosis in aging myocardial ischemia/reperfusion injury.

Myocardial ischemia/reperfusion (I/R) injury is a classic type of cardiovascular disease characterized by injury to cardiomyocytes leading to different types of cell death. The degree of irreversible myocardial damage is closely related to age, and ferroptosis is involved in cardiomyocyte damage. However, the mechanisms underlying ferroptosis regulation in aging myocardial I/R injury are still unclear. The present study aims to explore the underlying mechanism of piRNA regulation in ferroptosis. Using left anterior descending coronary artery ligation in an aging rat model and a D-galactose-induced rat cardiomyocyte line (H9C2) to construct an aging cardiomyocyte model, we investigate whether ferroptosis occurs after reperfusion injury in vitro and in vivo. This study focuses on the upregulation of piR-000699 after hypoxia/reoxygenation treatment in aging cardiomyocytes by observing hypoxia/reoxygenation (H/R) injury indicators and ferroptosis-related indicators and clarifying the role of piR-000699 in H/R injury caused by ferroptosis in aging cardiomyocytes. Bioinformatics analysis reveals that SLC39A14 is a gene that binds to piR-000699. Our data show that ferroptosis plays an important role in I/R injury both in vivo and in vitro. Furthermore, the results show the potential role of piR-000699 in regulating SLC39A14 in ferroptosis in aging cardiomyocytes under hypoxia/reoxygenation conditions. Together, our results reveal that the mechanism by which piR-000699 binds to SLC39A14 regulates ferroptosis in aging myocardial I/R injury.

The HN protein of Newcastle disease virus induces cell apoptosis through the induction of lysosomal membrane permeabilization.

Lysosomes are acidic organelles that mediate the degradation and recycling of cellular waste materials. Damage to lysosomes can cause lysosomal membrane permeabilization (LMP) and trigger different types of cell death, including apoptosis. Newcastle disease virus (NDV) can naturally infect most birds. Additionally, it serves as a promising oncolytic virus known for its effective infection of tumor cells and induction of intensive apoptotic responses. However, the involvement of lysosomes in NDV-induced apoptosis remains poorly understood. Here, we demonstrate that NDV infection profoundly triggers LMP, leading to the translocation of cathepsin B and D and subsequent mitochondria-dependent apoptosis in various tumor and avian cells. Notably, the released cathepsin B and D exacerbate NDV-induced LMP by inducing the generation of reactive oxygen species. Additionally, we uncover that the viral Hemagglutinin neuraminidase (HN) protein induces the deglycosylation and degradation of lysosome-associated membrane protein 1 (LAMP1) and LAMP2 dependent on its sialidase activity, which finally contributes to NDV-induced LMP and cellular apoptosis. Overall, our findings elucidate the role of LMP in NDV-induced cell apoptosis and provide novel insights into the function of HN during NDV-induced LMP, which provide innovative approaches for the development of NDV-based oncolytic agents.

Macrophage death induced cellular mechanisms and some regulatory pathways of macrophage death related diseases

In mammalian physiology the dead cells of body and cellular debris could not be digested by body’s own cellular mechanism. Macrophage is a component living inside the cell sometimes engulf the unrequired cell debris by phagocytosis and became dead by its own, this type of death inside macrophage is called ‘‘Macrophage Death’’ which has been done for our good cytosolic condition. Macrophage death is about many types those have been disclosed later and referred as ‘‘Programmed Cell Death.’’Apoptosis, Autophagy, Necrophagy all are different types of cell death associated with macrophage. When cytotoxicity of a cell condition leads to a cell destroy by its own then often it’s referred as a ‘‘Cellular Suicide’’ where cells die by itself.Macrophages death is a complicated mechanism which directly involves with ER stress, oxidative stress, lost mitochondrial functional ability, lysosomal outburst and other cell particulates dysfunctioning.

Is Intestinal Cell Death in Necrotising Enterocolitis Assorted and Multifarious? A Special Focus on Risk Factors and Their Pathogenic Mechanisms

Necrotising enterocolitis (NEC) is a serious gastrointestinal clinical disorder primarily affecting preterm newborns. It is characterised by a wider histological spectrum, ranging from mild mucosal injury, microvascular thrombosis, and localised necrosis, to transmural intestinal necrosis. In the most severe form, it can be fatal, with complications such as intestinal perforation, peritonitis, and sepsis. Medical management is not clinically efficacious except in mild and self-limiting cases, as it is only focused on symptomatic treatment. Intestinal cell death is regarded as a crucial nascent cellular event in the pathogenesis of NEC that leads to a leaky intestinal barrier, as well as local and systemic inflammation. Therefore, cellular events that besiege intestinal cell death in NEC should be understood in a meticulous and precise manner. This review provides an extensive overview of the different types of cell death in NEC, including apoptosis, necrosis, autophagy, necroptosis, and pyroptosis. This is critically important as it helps us to comprehend the downstream signalling events that play a vital role in the initiation and progression of disease in NEC. Pertinent research studies performed in this regard would unravel novel molecular targets that could form the basis for drafting innovative therapeutic agents for optimising clinical outcomes in NEC.

Is Intestinal Cell Death in Necrotising Enterocolitis Assorted and Multifarious? A Special Focus on Risk Factors and Their Pathogenic Mechanisms

Necrotising enterocolitis (NEC) is a serious gastrointestinal clinical disorder primarily affecting preterm newborns. It is characterised by a wider histological spectrum, ranging from mild mucosal injury, microvascular thrombosis, and localised necrosis, to transmural intestinal necrosis. In the most severe form, it can be fatal, with complications such as intestinal perforation, peritonitis, and sepsis. Medical management is not clinically efficacious except in mild and self-limiting cases, as it is only focused on symptomatic treatment. Intestinal cell death is regarded as a crucial nascent cellular event in the pathogenesis of NEC that leads to a leaky intestinal barrier, as well as local and systemic inflammation. Therefore, cellular events that besiege intestinal cell death in NEC should be understood in a meticulous and precise manner. This review provides an extensive overview of the different types of cell death in NEC, including apoptosis, necrosis, autophagy, necroptosis, and pyroptosis. This is critically important as it helps us to comprehend the downstream signalling events that play a vital role in the initiation and progression of disease in NEC. Pertinent research studies performed in this regard would unravel novel molecular targets that could form the basis for drafting innovative therapeutic agents for optimising clinical outcomes in NEC.

The exploration of mitochondrial-related features helps to reveal the prognosis and immunotherapy methods of colorectal cancer.

Cancer cell survival, proliferation, and metabolism are all intertwined with mitochondria. However, a complete description of how the features of mitochondria relate to the tumor microenvironment (TME) and immunological landscape of colorectal cancer (CRC) has yet to be made. We performed subgroup analysis on CRC patient data obtained from the databases using non-negative matrix factorization (NMF) clustering. Construct a prognostic model using the mitochondrial-related gene (MRG) risk score, and then compare it to other models for accuracy. Comprehensive analyses of the risk score, in conjunction with the TME and immune landscape, were performed, and the relationship between the model and different types of cell death, radiation and chemotherapy, and drug resistance was investigated. Results from immunohistochemistry and single-cell sequencing were utilized to verify the model genes, and a drug sensitivity analysis was conducted to evaluate possible therapeutic medicines. The pan-cancer analysis is utilized to further investigate the role of genes in a wider range of malignancies. We found that CRC patients based on MRG were divided into two groups with significant differences in survival outcomes and TME between groups. The predictive power of the risk score was further shown by building a prognostic model and testing it extensively in both internal and external cohorts. Multiple immune therapeutic responses and the expression of immunological checkpoints demonstrate that the risk score is connected to immunotherapy success. The correlation analysis of the risk score provide more ideas and guidance for prognostic models in clinical treatment. The TME, immune cell infiltration, and responsiveness to immunotherapy in CRC were all thoroughly evaluated on the basis of MRG features. The comparative validation of multiple queues and models combined with clinical data ensures the effectiveness and clinical practicality of MRG features. Our studies help clinicians create individualized treatment programs for individuals with cancer.

Circulating sNinj1 as a novel predictor of prognosis and severity in hepatocellular carcinoma

BackgroundThe occurrence and development of HCC are closely associated with cell death. Recently, researchers found that Ninj1 plays a pivotal role in PMR during different types of cell death. However, the importance of Ninj1 in HCC has not been extensively investigated. MethodsThis study included 102 newly diagnosed HCC patients and 102 sex and age-matched NCs. Circulating sNinj1 was assessed by ELISA. Serum LDH and IL-1ß were detected through a chemiluminescence assay. The correlations of these biomarkers with disease severity and their potential as prognostic predictors for HCC were evaluated. The dynamic changes of sNinj1, LDH, and IL-1ß levels before and after treatment were recorded. ResultsSerum levels of sNinj1, IL-1ß, and LDH were significantly higher in HCC patients. Our study found that the sNinj1 level was positively correlated with tumor size, metastasis, and staging. ROC analysis indicated that the AUC of sNinj1 in differentiating HCC from NCs was 0.85. As a result of tumor thrombosis and invasion of the hepatic vein, sNinj1′s AUCs were 0.71 and 0.73, respectively. After partial resection and TACE treatment, serum sNinj1 and LDH exhibited similar change trends. A one-year follow-up analysis also demonstrated that HCC patients with high sNinj1 had significantly poorer survival than those with low sNinj1. ConclusionsThe serum sNinj1 is another diagnostic biomarker supporting the HCC diagnosis. More importantly, it has been shown that circulating sNinj1 reveals potential as a novel predictor of HCC severity and prognosis.

In vitro siRNA-mediated GPX4 and AKT1 silencing in oxaliplatin resistance cancer cells induces ferroptosis and apoptosis.

Oxaliplatin is a member of platinum-based chemotherapy drugs frequently used in colorectal cancer (CRC). However, resistance to oxaliplatin causes tumor progression and metastasis. Akt1 and Gpx4 are essential regulator genes of apoptosis and ferroptosis pathways. Inhibition of these genes might eradicate oxaliplatin resistance in resistant CRC cells. We compared two cell death strategies to reverse drug resistance in Caco-2 and HT-29 oxaliplatin-resistant cell lines. We used the AKT1-specific siRNA to induce apoptosis. Also, GPX4-specific siRNA and FIN56 were utilized to generate ferroptosis. The effect of these treatments was assessed by reactive oxygen species (ROS) formation, cell viability, and protein expression level assays. Besides, the expression of GPX4, CoQ10, and NRF2 was assessed in both cell lines after treatments. Correctly measuring the expression of these responsible genes and proteins confirms the occurrence of different types of cell death. In addition, the ability of Akt1/ GPX4 siRNA in resensitizing HT-29 and Caco-2 oxaliplatin resistance cells was evaluated. Our finding showed that the upregulation of GPX4/siRNA caused a reduction in GPX4 and CoQ10 expressions in both cell lines. However, the expression level of NRF2 showed the same level in our cell lines, so we observed a downregulation of NRF2 in resistant CRC cell lines. Cell viability assay indicated that induction of ferroptosis by GPX4/siRNA or FIN56 and apoptosis by Akt1/siRNA in resistant cell lines could reverse the oxaliplatin resistance. We concluded that downregulation of Akt1 or Gpx4 could increase the efficacy of oxaliplatin to overcome the resistance compared to FIN56.

The Effect of Natural Substances Contained in Bee Products on Prostate Cancer in In Vitro Studies.

Prostate cancer is a common cancer in men in older age groups. The WHO forecasts an increase in the incidence of prostate cancer in the coming years. Patients may not respond to treatment, and may not tolerate the side effects of chemotherapy. Compounds of natural origin have long been used in the prevention and treatment of cancer. Flavonoids obtained from natural products, e.g., propolis, are compounds with proven antibacterial and antiviral efficacy which modulate the immune response and may be useful as adjuvants in chemotherapy. The main aim of the present study was to evaluate the cytotoxic and pro-apoptotic properties of selected flavonoids on prostate cancer cells of the LNCaP line. The compounds used in this study were CAPE, curcumin (CUR), and quercetin (QUE). Mitochondrial and lysosome metabolism was assessed by the XTT-NR-SRB triple assay as well as by the fluorescent staining techniques. Staining for reactive oxygen species was performed as well. The experiment showed that each of the tested compounds has a cytotoxic effect on the LNCaP cell line. Different types of cell death were induced by the tested compounds. Apoptosis was induced by quercetin, while autophagy-specific changes were observed after using CAPE. Compounds obtained from other bee products have antiproliferative and cytotoxic activity against LNCaP prostate cancer cells.

The metabolite alpha-ketoglutarate: a novel target of gasdermin C-dependent pyroptosis.

The metabolite alpha-ketoglutarate: a novel target of gasdermin C-dependent pyroptosis.

An overview of programmed cell death: Apoptosis and pyroptosis-Mechanisms, differences, and significance in organism physiology and pathophysiology.

Regulated cell death is an essential and heterogeneous process occurring in the life cycle of organisms, from embryonic development and aging to the regulation of homeostasis and organ maintenance. Under this term, we can distinguish many distinct pathways, including apoptosis and pyroptosis. Recently, there has been an increasing comprehension of the mechanisms governing these phenomena and their characteristic features. The coexistence of different types of cell death and the differences and similarities between them has been the subject of many studies. This review aims to present the latest literature in the field of pyroptosis and apoptosis and compare their molecular pathway's elements and significance in the physiology and pathophysiology of the organism.

Higher β cell death in pregnant women, measured by DNA methylation patterns of cell-free DNA, compared to new-onset type 1 and type 2 diabetes subjects: a cross-sectional study

Diabetes is a metabolic disorder of glucose homeostasis in which β cell destruction occurs silently and is detected mainly when symptoms appear. In the last few years, it has emerged a great interest in developing markers capable of detecting pancreatic β cell death focused on improving early diagnosis and getting a better treatment response, mainly in type 1 diabetes. But other types of diabetes would also benefit from early detection of β cell death. Differentially methylated circulating DNA is being studied as minimally invasive biomarker of cell death. We aimed to explore whether the unmethylated/methylated ratio of the insulin and amylin genes might be a good biomarker of β cell death in different types of diabetes. A lower index ∆Ct indicates a higher rate of β-cell death. Plasma samples from subjects without diabetes, pregnant women, pregnant with gestational diabetes (GDM), type 1 diabetes and type 2 diabetes were analyzed. A qPCR reaction with specific primers for both methylated and unmethylated fragments of insulin and amylin genes were carried out. Pregnant women, GDM and non- GDM, showed a higher β-cell death for both markers (∆INS = 3.8 ± 2.1 and ∆Amylin = 8.5 ± 3.6), whereas T1D presented lower rate (∆INS = 6.2 ± 2.1 and ∆Amylin = 10.7 ± 2.9) comparable to healthy subjects. The insulin methylation index was associated with the newborn birth weight (r = 0.46; p = 0.033) and with insulin resistance (r = -0.533; p = 0.027) in the GDM group. The higher rate of β-cell death was observed in pregnant women independently of their metabolic status. These indexes could be a good indicator of β cell death in processes caused by defects on insulin secretion, insulin action, or both.

Novel Insights in the Potential of Halogenated Polyketide–Peptide Molecules as Lead Compounds in Cancer Drug Discovery

In this interdisciplinary study, we selected two compounds, namely, smenamide A, a peptide-polyketide, and smenolactone D, a polyketide, as models because they are representative of two different classes of molecules isolated from the marine sponge Smenospongia aurea. The organic extract of Smenospongia aurea was analyzed using a combination of high-resolution LC-MS/MS and molecular networking, a recently developed method for automated LC-MS data analysis. The analyses were targeted to highlight clusters made by chlorinated compounds present in the extracts. Then, the two model compounds were analyzed for their bioactivity. Data reported here show that smenamide A did not exhibit a cytotoxic effect, while smenolactone D was cytotoxic on different tumor cell lines and was able to induce different types of cell death, including ferroptosis and apoptosis.

L-kynurenine induces NK cell loss in gastric cancer microenvironment via promoting ferroptosis

BackgroundNatural killer (NK) cells play a major role in body’s fighting against various types of cancers. Their infiltration in the tumor microenvironment (TME) of gastric cancer (GC) are significantly decreased, which has been reported as a robust prognostic marker. However, the causes leading to NK cells loss in GC TME remains poorly understood.MethodsWe constructed a non-contact co-culturing system and humanized xenograft tumor mice model to detect the influence of GC microenvironment on NK-92 or primary human NK cells viability by flow cytometry. Then through using the specific inhibitors for different types of cell death and examining the surrogate markers, we confirmed ferroptosis in NK cells. Inspired by the accidental discoveries, we constructed a NK-92 cell strain with high expression of GPX4 and treated the humanized xenograft tumor mice model with the NK-92 cells.ResultsWe found L-KYN, mainly generated through indoleamine 2, 3-dioxygenase (IDO) from GC cells, impaired NK cells viability in TME. Further analysis revealed L-KYN induced ferroptosis in NK cells via an AHR-independent way. Moreover, we found NK cells with higher GPX4 expression showed resistance to L-KYN induced ferroptosis. Based on this, we generated GPX4 over-expressed NK-92 cells, and found these cells showed therapeutic potential towards GC.ConclusionsOur study revealed a novel mechanism to explain the decline of NK cell number in GC TME. Notably, we also developed a potential immunotherapy strategy, which might be beneficial in clinical treatment in the future.

NETosis and kidney disease: what do we know?

Neutrophils are the most abundant leukocytes in the blood. They are rapidly mobilized from the circulation to sites of inflammation and/or infection. In affected tissues, neutrophils exhibit some dramatic antimicrobial functions, including degranulation, reactive oxygen species (ROS) production, phagocytosis, and formation of neutrophil extracellular traps (NETs). Like other cells of the immune system, after fulfilling their biological duties, they enter the path of death. Depending on the conditions, they may undergo different types of cell death (apoptosis, necrosis, necroptosis, autophagy, NETosis, and pyroptosis) that require the participation of multiple signaling pathways. NETosis is a unique neutrophil cell death mechanism that gives rise to different inflammatory and autoimmune pathological conditions. Recent studies have shown that NETosis also plays a role in the formation and/or progression of kidney diseases. This review discusses the underlying mechanism of NETosis and its relationship with some major kidney diseases in light of the current knowledge.