Regulated cell death (RCD) has emerged as a pivotal upstream mediator supported by correlative preclinical and clinical evidence in the pathogenesis of sepsis-induced coagulopathy (SIC), a life-threatening complication strongly linked to increased mortality. RCD-guided phenotyping integrates pyroptosis, NETosis, ferroptosis, necroptosis, and PANoptosis pathways to systematically redefine SIC — from molecular signatures to targeted interventions. This review comprehensively examines how RCD-derived Damage-Associated Molecular Patterns (DAMPs) mediate coagulation dysfunction, explores subtype-specific biomarkers for patient stratification, and outlines phenotype-directed combination therapies. We further investigate unresolved challenges and future developments in RCD-guided precision immunomodulation, emphasizing the transformative potential of RCD-based frameworks to advance the clinical management of SIC by bridging insights from cell death and thrombosis research. Regulated Cell Death-induced Coagulation Dysfunction in Sepsis This graphical abstract summarizes the core framework of the review. (1) Clinical Issues: Sepsis progresses to sepsis-induced coagulopathy (SIC) and disseminated intra-vascular coagulation (DIC), with conventional single-target therapies showing limited efficacy. (2) Core Mechanism: Regulated cell death (RCD) activation triggers the release of damage-associated molecular patterns (DAMPs), which drive coagulation dysfunction. (3) Subtyping Therapy Module: Based on distinct molecular signatures, SIC can be stratified into four RCD-dominant phenotypes, enabling phenotype-directed targeted therapy. (4) Translational Challenges: Clinical translation is hindered by three key obstacles: unvalidated bi-omarkers, undefined therapeutic time windows, and potential off-target effects of systemic interventions.

BACKGROUND:Acute pancreatitis (AP) is a severe inflammatory disorder characterized by pancreatic self-digestion, often progressing to systemic inflammation. Despite advances in understanding its pathogenesis, effective therapeutic strategies remain limited. Heat shock factor 1 (HSF1), a critical transcription factor that maintains cellular homeostasis and regulates the stress response, is downregulated in the pancreas of L-arginine-induced AP mice. However, its role and regulatory mechanisms in the pathogenesis of AP remain unclear. This study aims to elucidate the molecular function and mechanisms of HSF1 in AP, focusing on its regulation by E1A binding protein p300 (EP300) and the downstream effects on mitophagy and inflammation. METHODS:Two distinct mouse models of AP were established using L-arginine and cerulein. Pancreatic acinar cells (AR42J) were used to study the effects of HSF1 and parkin RBR E3 ubiquitin protein ligase (PRKN) on mitophagy and inflammation. The expression and regulation between HSF1, PRKN, and EP300 were assessed using genetic and pharmacological approaches. RESULTS:HSF1 deficiency exacerbates AP severity in two distinct mouse models, with increased mortality, pancreatic necrosis, and systemic inflammation. Mechanistically, HSF1 directly binds to the promoter of PRKN, enhancing its transcriptional activity. Thus, HSF1 alleviates the inflammatory response in pancreatic acinar cells during AP by promoting PRKN-mediated mitophagy, reducing ROS production, and inhibiting NLRP3 inflammasome activation. HSF1 expression is downregulated in pancreatic acinar cells due to decreased acetylation by EP300, leading to proteasomal degradation and impaired mitophagy. Pharmacological activation of EP300 (e.g., CTB) restores HSF1 expression, enhances mitophagy, and attenuates inflammation in both in vivo and in vitro settings. CONCLUSION:These findings highlight the critical role of EP300 in regulating HSF1 acetylation and stability, which in turn modulates mitophagy and pyroptosis in AP. Targeting EP300 and its downstream pathways, such as HSF1-PRKN axis, may offer novel therapeutic strategies for AP.

Introduction: Infection and coagulation dysfunction are two major features of sepsis, and TFPI2 exhibits both antimicrobial and anticoagulant properties. This study aims to evaluate whether TFPI2 is associated with the severity of sepsis, thereby determining its potential value in sepsis diagnosis and prognosis. Methods: Serum TFPI2 concentrations were measured and compared among 32 healthy controls, 16 intensive care unit (ICU) nonsepsis patients, and 106 ICU sepsis patients. Correlation analysis was performed between various indicators and TFPI2 levels in sepsis patients. Logistic regression analysis and receiver operating characteristic curves were used to assess the value of TFPI2 in predicting 28-day mortality in sepsis. Results: Sepsis patients exhibited markedly elevated serum TFPI2 levels compared with both healthy individuals and ICU patients without sepsis. Serum TFPI2 levels were significantly correlated with sepsis severity indicators such as Sequential Organ Failure Assessment score, Acute Physiology and Chronic Health Evaluation II score, Lac, coagulation markers including International Society on Thrombosis and Hemostasis overt disseminated intravascular coagulation criteria and Sepsis-Induced Coagulopathy scores, and platelet count. Univariate and multivariate logistic regression analyses revealed that TFPI2 is an independent risk factor for 28-day mortality in sepsis. The receiver operating characteristic curve showed that TFPI2 has a significant predictive value for 28-day mortality in sepsis, with an area under the curve of 0.832 and an optimal cutoff value of 8.316. Conclusions: This study indicates that serum TFPI2 levels hold promise as a biomarker for predicting the severity of sepsis.

Recent studies prove that the three well-established cell death pathways-pyroptosis, apoptosis, and necroptosis-are not isolated but rather engage in extensive crosstalk. PANoptosis, a newly identified pathway of inflammatory regulated cell death (RCD), integrates characteristics of apoptosis, pyroptosis, and necroptosis. Caspases are a family of conserved cysteine proteases that play critical roles in pyroptosis, apoptosis, and necroptosis. Similarly, caspases also play a role in PANoptosis. In this paper, we review the molecular mechanisms of these three RCDs and the crosstalk between them. We also delineate the discovery of PANoptosis and its association with disease. Furthermore, we discuss the caspase function in PANoptosis, mainly focusing on caspase-6 and caspase-8 molecules. This review describes the key molecules, especially caspases, in the context of PANoptosis research, aiming to provide a foundation for targeted interventions in PANoptosis-associated diseases.

Immune cell metabolic reprogramming toward glycolysis is vital for sepsis defense. While interleukin 1 receptor 2 (IL1R2) acts as a decoy receptor for IL1α/β, its potential impact on cell metabolism and death during sepsis remains unclear. This study observed elevated plasma soluble IL1R2 (sIL1R2) levels in septic patients and mice. In pyroptotic macrophages, reduced intracellular IL1R2 expression led to its release extracellularly. Proteomic screening identified enolase 1 (ENO1), a key glycolysis enzyme, as the binding partner of IL1R2 in macrophages. IL1R2 suppresses ENO1 activity to inhibit glycolysis, gasdermin D (GSDMD)-mediated pyroptosis, and inflammation in macrophages. IL1R2-deficient mice exhibited heightened susceptibility to sepsis, with increased inflammation, organ injury, and mortality. Notably, ENO1 inhibition reduced inflammation, organ injury, and improved survival rates in septic mice. The study reveals that IL1R2 interacts with ENO1 to inhibit glycolysis-mediated pyroptosis and inflammation in sepsis, suggesting the IL1R2-ENO1 interaction as a promising therapeutic target of sepsis.

Background: Multiple cell death modalities are implicated in sepsis pathobiology. However, the clinical relevance of NINJ1, a key mediator of plasma membrane rupture during lytic cell death, in sepsis progression and outcomes has remained poorly explored. Methods: Circulating NINJ1 levels were measured in 116 septic intensive care unit (ICU) patients, 16 nonseptic ICU controls, and 16 healthy controls. Comparative analysis of serum NINJ1 across these groups was performed. Correlations between NINJ1 and clinical disease severity scores (Sequential Organ Failure Assessment [SOFA], Acute Physiology and Chronic Health Evaluation [APACHE II]) as well as laboratory parameters were examined in the sepsis cohort. Furthermore, we assessed the prognostic performance of NINJ1 for predicting 28-day mortality in septic patients using receiver operating characteristic (ROC) analyses. Results: Circulating NINJ1 levels were elevated in septic patients and positively correlated with sepsis severity scores. NINJ1 also showed positive correlations with liver injury markers (aspartate transaminase/alanine aminotransferase) and coagulation parameters (D-dimer, activated partial thromboplastin time, prothrombin time, thrombin time) in sepsis. Further analysis using the International Society on Thrombosis and Hemostasis overt disseminated intravascular coagulation scoring system revealed an association between NINJ1 and sepsis-induced coagulopathy. ROC analysis demonstrated that NINJ1 outperformed traditional inflammatory biomarkers procalcitonin and C-reactive protein in predicting 28-day sepsis mortality, although its prognostic accuracy was lower than SOFA and APACHE II scores. Combining NINJ1 with SOFA improved mortality prediction from an area under the curve of 0.6843 to 0.773. Conclusions: Circulating NINJ1 serves as a novel sepsis biomarker indicative of disease severity, coagulopathy and mortality risk, and its integration with SOFA and APACHE II scores substantially enhances prognostic risk stratification. These findings highlight the prospective clinical utility of NINJ1 for sepsis prognostication and monitoring, warranting further validation studies to facilitate implementation.

Objective To study the effects of HSP70 on proliferation, migration, invasion, and epithelial-mesenchymal transformation (EMT) of pancreatic cancer cells and explore its underlying mechanisms. Methods Pancreatic cancer cell models with reduced HSP70 or increased HSP70 expression were established. Reverse transcription quantitative polymerase chain reaction and Western blot assays were used to determine mRNA and protein levels of HSP70, IKK/IκBa/NF-κB signaling pathway-related genes, and EMT markers. CCK-8 and cell cloning assays were used to evaluate cell proliferation and cloning abilities. Transwell and wound healing assays were used to assess the invasive and migratory properties of cells. Electrophoresis mobility shift assay (EMSA) and luciferase reporter assays were conducted to analyze NF-κB's promoter binding and transcriptional activities. Results HSP70 knockdown inhibited p-p65 nuclear translocation, the expression of p-p65, p-IKKα/β, p-IκBα, N-cadherin, Vimentin and Twist, NF-κB's promoter binding and transcriptional activities, pancreatic cancer cell proliferation, cloning, migration and invasion, while increased E-cadherin levels. HSP70 overexpression took the opposite effects. NF-κB signaling pathway modulation reversed EMT changes induced by altered HSP70 expression levels. rhHSP70 increased p-IKKα/β and p-IκBα protein levels. Conclusions HSP70 promotes EMT and enhances pancreatic cancer cell proliferation, migration, and invasion by activating NF-κB pathway.

As an uncontrolled inflammatory response to infection, sepsis and sepsis induced organ dysfunction are great threats to the lives of septic patients. Unfortunately, the pathogenesis of sepsis is complex and multifactorial, which still needs to be elucidated. Pyroptosis is a newly discovered atypical form of inflammatory programmed cell death, which depends on the Caspase-1 dependent classical pathway or the non-classical Caspase-11 (mouse) or Caspase-4/5 (human) dependent pathway. Many studies have shown that pyroptosis is related to sepsis. The Gasdermin proteins are the key molecules in the membrane pores formation in pyroptosis. After cut by inflammatory caspase, the Gasdermin N-terminal fragments with perforation activity are released to cause pyroptosis. Pyroptosis is closely related to the occurrence and development of sepsis induced organ dysfunction. In this review, we summarized the molecular mechanism of pyroptosis, the key role of pyroptosis in sepsis and sepsis induced organ dysfunction, with the aim to bring new diagnostic biomarkers and potential therapeutic targets to improve sepsis clinical treatments.

Background: Endoscopic retrograde cholangiopancreatography (ERCP) is a minimally invasive technique widely used to diagnose and treat pancreatic and biliary diseases; however, it is linked with imminent hyperamylasemia and post-ERCP pancreatitis (PEP). Somatostatin and indomethacin are the classic recommended drugs used for PEP prevention. Objective: To elucidate the effects of somatostatin and indomethacin mono or in combination to prevent hyperamylasemia and PEP in high-risk individuals. Methods: Altogether 1458 patients who underwent ERCP in our hospital from January 2016 to May 2022 were included in this investigation and categorized into 4 groups based on the treatment regimen: placebo, indomethacin, somatostatin, and indomethacin + somatostatin. The pre operation and post operation (at 6, 12, and 24 h) hospitalization cost, length of stay, the occurrence of hyperamylasemia and PEP, levels of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), IL-8, and VAS pain score were determined in the 4 groups. In all the groups, VAS and IL-6, TNF-α, and IL-8 levels substantially increased in the pretreatment and decreased sequentially from 6 to 24 h post operation. The individuals in the indomethacin revealed substantially reduced hyperamylasemia, VAS, and levels of IL-6, TNF-α, and IL-8, 6 h post operation, whereas the hospitalization fee, length of stay, PEP incidence, VAS, levels of IL-6, TNF-α, and IL-8, 12 and 24 h post operation were not statistically important in comparison with the individuals who received placebo therapy. The somatostatin and the indomethacin + somatostatin groups indicated markedly alleviated hospitalization fee, length of stay, the occurrence of hyperamylasemia and PEP, VAS, and the levels of IL-6, TNF-α, and IL-8 at 6, 12, and 24 h post operation compared with the placebo cohort. Furthermore, compared with the indomethacin group, the above-determined factors notably reduced at 6, 12, and 24 h post operation in somatostatin and indomethacin + somatostatin groups. It was also observed that the indomethacin + somatostatin group has substantially decreased the occurrence of hyperamylasemia, VAS score, and levels of IL-6, TNF-α, and IL-8, 6 hours post operation, while at 12 and 24 h post operation, the hospitalization fee, length of stay and incidence of PEP, VAS, levels of IL-6, TNF-α, and IL-8 were not statistically important compared with the somatostatin group. It is also worth noting that the side effects of both drugs are rare and mild. Results: For high-risk PEP patients, indomethacin and somatostatin can efficiently alleviate post-operative hyperamylasemia and improve their life standard within 6 hours and 24 hours, respectively. Indomethacin is suitable for individuals who underwent simple, short-duration ERCP with expected mild post-operative abdominal pain, whereas somatostatin is given to patients with complicated, long-duration ERCP and expected severe post-operative abdominal pain. Their combinational therapy produces a synergistic effect and can reduce the incidence of hyperamylasemia, thereby improving patients’ quality of life within 6 h and is also effective against individuals who received a more complicated, longer-duration ERCP and were expected to have severer and longer post-operative abdominal pain.

OBJECTIVE:To investigate the GSDMD, CASP1, CASP4 and CASP5 expression in peripheral blood mononuclear cells of non-small cell lung cancer patients and analyze their clinical significance. METHODS:71 non-small cell lung cancer patients were selected as the study group and 50 healthy individuals as the control group. The GSDMD, CASP1, CASP4 and CASP5 expression in peripheral blood mononuclear cells of the two groups were detected by real-time fluorescence quantitative PCR. The GSDMD, CASP1, CASP4, CASP5 expression and their relationship with the clinical characteristics of the patients were analyzed. RESULTS:Compared with the control group, the GSDMD, CASP4 and CASP5 expression in PBMCs of lung cancer patients was significantly higher(P < 0.05). Lymph node metastasis had significant difference with the CASP4 and GSDMD expression (P < 0.05); tumor volume had significant difference with CASP1 and CASP5 expression (P < 0.05). The areas under predictive ROC curve of the GSDMD, CASP1, CASP4, and CASP5 mRNA expression were 0.629(P < 0.05), 0.574(p > 0.05), 0.701(P < 0.05) and 0.628(P < 0.05), the sensitivity values were 84.5%, 67.6% 43.7%, and 84.3%;the specificity values were 42%, 52%, 84% and 64%, respectively. CONCLUSION:GSDMD, CASP1, CASP4 and CASP5 gene expression are highly increased in PBMCs of non-small cell lung cancer patients and their expression are closely related to the clinical characteristics of patients. The early enhanced pyroptosis-related gene expression may be potential molecular markers for early diagnosis of non-small cell lung cancer.

Diabetes mellitus (DM) is a metabolic inflammatory disease with a high incidence worldwide. Patients with DM are at a high risk for all types of infections. Type 1 DM is characterised with immune destruction of pancreatic β cells, while type 2 diabetes is characterised with insulin resistance and β cell dysfunction, both of which result in disorders of glucose and lipid metabolism. This metabolic disorder causes functional defects of immune cells, aberrant production of inflammatory cytokines, dysregulated immune responses, advanced pathophysiological injury of the body, and increased mortality in populations with DM upon infections. Starting with the change of natural immune system in patients with DM, this paper focused on the enhanced severity of infections in DM and the underlying innate immune alterations in preclinical and clinical studies, aiming to better understand the influence of DM on the susceptibility, pathophysiology, and clinical outcomes in infections.

Objective: To screen and validate reference genes suitable for gene mRNA expression study in peripheral blood mononuclear cells (PBMCs) between septic patients and healthy controls (HC). Methods: Total RNA in PBMCs was extracted and RT-qPCR was used to determine the mRNA expression profiles of 9 candidate genes, including ACTB, B2M, GAPDH, GUSB, HPRT1, PGK1, RPL13A, SDHA and YWHAZ. The genes expression stabilities were assessed by both geNorm and NormFinder software. Results: YWHAZ was the most stable gene among the 9 candidate genes evaluated by both geNorm and NormFinder in mixed and sepsis groups. The most stable gene combination in mixed group analyzed by geNorm was the combination of GAPDH, PKG1 and YWHAZ, while that in sepsis group was the combination of ACTB, PKG1 and YWHAZ. Conclusion: Our first systematic analysis of the reference genes in PBMC of septic patients suggested YWHAZ was the best candidate. The combination of ACTB, PKG1 and YWHAZ could improve RT-qPCR accuracy in septic patients. Our results identified the most stable reference genes to standardize RT-qPCR of sepsis patients, which can serve as a useful tool for gene function exploration in the future.

Background. Sepsis, which could cause a systemic inflammatory response, is a life-threatening disease with a high morbidity and mortality rate. There is evidence that brain injury may be related to severe systemic infection induced by sepsis. The brain injury caused by sepsis could increase the risk of mortality in septic patients, which seriously affects the septic patient’s prognosis of survival. Although there remains a focus on sepsis research, clinical measures to prevent and treat brain injury in sepsis are not yet available, and the high mortality rate is still a big health burden. Therefore, it is necessary to investigate the new molecules or regulated pathways that can effectively inhibit the progress of sepsis. Objective. NLR family pyrin domain-containing 3 (NLRP3) increased in the procession of sepsis and functioned as the key regulator of pyroptosis. Heat shock factor 1 (HSF1) can protect organs from multiorgan dysfunction syndrome induced by lipopolysaccharides in mice, and NLRP3 could be inhibited by HSF1 in many organs. However, whether HSF1 regulated NLRP3 in sepsis-induced brain injury, as well as the detailed mechanism of HSF1 in brain injury, remains unknown in the sepsis model. In this research, we try to explore the relationship between HSF1 and NLRP3 in a sepsis model and try to reveal the mechanism of HSF1 inhibiting the process of brain injury. Methods. In this study, we used wild-type mice and hsf1-/- mice for in vivo research and PC12 cells for in vitro research. Real-time PCR and Western blot were used to analyze the expression of HSF1, NLRP3, cytokines, and pyrolytic proteins. EthD-III staining was chosen to detect the pyroptosis of the hippocampus and PC12 cells. Results. The results showed that HSF1 is negatively related to pyroptosis. The pyroptosis in cells of brain tissue was significantly increased in the hsf1-/- mouse model compared to hsf1+/+ mice. In PC12 cells, hsf1 siRNA can upregulate pyroptosis while HSF1-transfected plasmid could inhibit the pyroptosis. HSF1 could negatively regulate the NLRP3 pathway in PC12 cells, while hsf1 siRNA enhanced the pyroptosis in PC12 cells, which could be reversed by nlrp3 siRNA. Conclusion. These results imply that HSF1 could alleviate sepsis-induced brain injury by inhibiting pyroptosis through the NLRP3-dependent pathway in brain tissue and PC12 cells, suggesting HSF1 as a potential molecular target for treating brain injury in sepsis clinical studies.

Recent investigations have shown that closed incisional negative pressure wound therapy (ciNPWT) decreases the rate of postoperative wound complications following revision total knee arthroplasty (TKA). In this study, we used a break-even analysis to determine whether ciNPWT is a cost-effective measure for reducing prosthetic joint infection (PJI) after revision TKA. The cost of ciNPWT, cost of treatment for PJI, and baseline infection rates following revision TKA were collected from institutional data and the literature. The absolute risk reduction (ARR) in infection rate necessary for cost-effectiveness was calculated using break-even analysis. Using our institutional cost of ciNPWT ($600), this intervention would be cost-effective if the initial infection rate of revision TKA (9.0%) has an ARR of 0.92%. The ARR needed for cost-effectiveness remained constant across a wide range of initial infection rates and declined as treatment costs increased. The use of ciNPWT for infection prevention following revision TKA is cost-effective at both high and low initial infection rates, across a broad range of treatment costs, and at inflated product expenses.

For the first time, increased Dp71 in ischemia-reperfusion injured rat heart were identified, both Dp71 mRNA and protein reached its peak expression 8 h after reperfusion. In H2O2 stimulated H9c2 cells, Dp71 mRNA and protein gradually increased and reached a peak at 16 h. Enhanced Dp71 in H9c2 could resist H2O2-induced cell apoptosis, while Dp71 depletion accelerated the apoptosis induced by H2O2. Enhanced Bcl-2 expression and Bcl-2∕Bax protein expression ratio was identified in Dp71 overexpressed H9c2 cells, while knocking down Dp71 significantly decreased the Bcl-2 and Bcl-2∕Bax protein expression ratio. Increased Dp71 can accelerate FAK and p65 phosphorylation, which finally resulted in enhanced Bcl-2 expression and explains the highly possible cardiac protection role of Dp71.

Myeloid-derived suppressor cells (MDSCs) mobilize and migrate from bone marrow to peripheral tissues or immune organs, which is associated with poor prognosis in sepsis. Intervention of MDSCs might be a potential target for the effective treatment of sepsis. In the present study, we demonstrated that IL-1R1 blockade with either recombinant human IL-1R antagonist Anakinra or IL-1R1 deficiency had a protective effect on the liver injury in septic mice. The possible mechanism was that Anakinra treatment and IL-1R1 knockout inhibited the migration of MDSCs to the liver in sepsis, thus attenuating the immune suppression of MDSCs on effector T cells characterized with the decrease in proportion of CD4+ and CD8+ T cells. Furthermore, the switch from pro-inflammatory M1 macrophage to anti-inflammatory M2 phenotype and the ability of bacterial clearance in the liver of septic mice were enhanced obviously by Anakinra and IL-1R1 deficiency, which contributes to the attenuated liver injury. Taken together, these findings provide new ideas for revealing the relationship between IL-1R1 and MDSCs in sepsis, thereby providing a potentially effective target for ameliorating septic liver injury.

As an important transcription factor, heat shock factor 1 (HSF1) plays an endogenous anti-inflammation role in the body and can alleviate multiple organ dysfunction caused by sepsis, which contributes to an uncontrolled inflammatory response. The NLRP3 inflammasome is a supramolecular complex that plays key roles in immune surveillance. Inflammation is accomplished by NLRP3 inflammasome activation, which leads to the proteolytic maturation of IL-1β and pyroptosis. However, whether HSF1 is involved in the activation of the NLRP3 inflammasome in septic acute lung injury (ALI) has not been reported. Here, we show that HSF1 suppresses NLRP3 inflammasome activation in transcriptional and post-translational modification levels. HSF1 can repress NLRP3 expression via inhibiting NF-κB phosphorylation. HSF1 can inhibit caspase-1 activation and IL-1β maturation via promoting NLRP3 ubiquitination. Our finding not only elucidates a novel mechanism for HSF1-mediated protection of septic ALI but also identifies new therapeutic targets for septic ALI and related diseases.

Objective: To study the serum expression level of heat shock proteins 70 (HSP70) and its relationship with radiotherapy sensitivity in pancreatic carcinoma.Methods: 168 patients with pancreatic cancer were enrolled between January 2019 and March 2021 from Southern Medical University Ping Xiang Hospital.Serum HSP70 and CA 19-9 levels were analyzed before, during, and post-radiotherapy.The receiver operating characteristic curve (ROC) was used for obtaining the predictive value of serum HSP70 level with radiotherapy sensitivity.Results: Serum levels of HSP70 were positively correlated with tumor diameter, stage, and lymph node metastasis but negatively correlated with the tumor grade.The concentration trend of HSP70 and CA 19-9 before treatment were: normal control group < complete response (CR) group < partial response (PR) group < stable disease (SD) group < progressive disease (PD) group.The concentrations of HSP70 in the CR, PR, and SD groups decreased after radiotherapy, while the concentrations of HSP70 in the PD group increased after the radiotherapy.The reduction percentage of HSP70 in the CR, PR, and SD groups was positively correlated with the reduction percentage of tumor diameter and CA 19-9.In contrast, the increase percentage of HSP70 in the PD group was positively correlated with the increase percentage in tumor diameter and CA 19-9.Conclusion: Serum HSP70 and CA 19-9 were positively correlated and closely related to the radiotherapy sensitivity of pancreatic cancer.Moreover, HSP70 and CA 19-9 can be used as biomarkers to predict radiotherapy sensitivity of pancreatic carcinoma.However, a combined diagnosis is better for sensitivity and specificity.

Ferroptosis is a novel form of cell death characterized by the iron-dependent accumulation of lipid peroxides and is different from other types of cell death. The mechanisms of ferroptosis are discussed in the review, including System Xc-, Glutathione Peroxidase 4 pathway, Ferroptosis Suppressor Protein 1 and Dihydroorotate Dehydrogenase pathway. Ferroptosis is associated with the occurrence of various diseases, including sepsis. Research in recent years has displayed that ferroptosis is involved in sepsis occurrence and development. Iron chelators can inhibit the development of sepsis and improve the survival rate of septic mice. The ferroptotic cells can release damage-associated molecular patterns and lipid peroxidation, which further mediate inflammatory responses. Ferroptosis inhibitors can resist sepsis-induced multiple organ dysfunction and inflammation. Finally, we reviewed ferroptosis, an iron-dependent form of cell death that is different from other types of cell death in biochemistry, morphology, and major regulatory mechanisms, which is involved in multiple organ injuries caused by sepsis. Exploring the relationship between sepsis and ferroptosis may yield new treatment targets for sepsis.