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Type 2 diabetes mellitus (T2DM) is a metabolic disorder with intricate pathogenic mechanisms. Despite the availability of various oral medications for controlling the condition, reports of poor glycemic control in type 2 diabetes persist, possibly involving unknown pathogenic mechanisms. In recent years, the gut microbiota have emerged as a highly promising target for T2DM treatment, with the metabolites produced by gut microbiota serving as crucial intermediaries connecting gut microbiota and strongly related to T2DM. Increasingly, traditional Chinese medicine is being considered to target the gut microbiota for T2DM treatment, and many of them are edible. In studies conducted on animal models, edible traditional Chinese medicine have been shown to primarily alter three significant gut microbiotal metabolites: short-chain fatty acids, bile acids, and branched-chain amino acids. These metabolites play crucial roles in alleviating T2DM by improving glucose metabolism and reducing inflammation. This review primarily summarizes twelve edible traditional Chinese medicines that improve T2DM by modulating the aforementioned three gut microbiotal metabolites, along with potential underlying molecular mechanisms, and also incorporation of edible traditional Chinese medicines into the diets of T2DM patients and combined use with probiotics for treating T2DM are discussed. [ABSTRACT FROM AUTHOR]

Objective: Sepsis and sepsis-associated organ failure are devastating conditions for which there are no effective therapeutic agent. Several studies have demonstrated the significance of ferroptosis in sepsis. The study aimed to identify ferroptosis-related genes (FRGs) in sepsis, providing potential therapeutic targets. Methods: The weighted gene co-expression network analysis (WGCNA) was utilized to screen sepsis-associated genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were used to explore gene functions. Three machine learning methods were employed to identify sepsis-related hub genes. Survival and multivariate Cox regression analysis allowed further screening for the key gene RRM2 associated with prognosis. The immune infiltration analysis of the screened sepsis key genes was performed. Additionally, a cecum ligation and puncture (CLP)-induced mouse sepsis model was constructed to validate the expression of key gene in the sepsis. Results: Six sepsis-associated differentially expressed FRGs (RRM2, RPL7A, HNRNPA1, PEBP1, MYL8B and TXNIP) were screened by WGCNA and three machine learning methods analysis. Survival analysis and multivariate Cox regression analysis showed that RRM2 was a key gene in sepsis and an independent prognostic factor associated with clinicopathological and molecular features of sepsis. Immune cell infiltration analysis demonstrated that RRM2 had a connection to various immune cells, such as CD4 T cells and neutrophils. Furthermore, animal experiment demonstrated that RRM2 was highly expressed in CLP-induced septic mice, and the use of Fer-1 significantly inhibited RRM2 expression, inhibited serum inflammatory factor TNF-α, IL-6 and IL-1β expression, ameliorated intestinal injury and improved survival in septic mice. Conclusion: RRM2 plays an important role in sepsis and may contribute to sepsis through the ferroptosis pathway. This study provides potential therapeutic targets for sepsis. [ABSTRACT FROM AUTHOR]

To elucidate the induction of ferroptotic pathways and the transcriptional modulation of pivotal genes in the context of hemorrhagic shock. The R software was used to analyze the GSE64711 dataset, isolating genes relevant to ferroptosis. Enrichment analyses and protein interaction networks were assembled. Using WGCNA hub genes were identified and intersected with ferroptosis-related genes, highlighting hub genes CD44 and MAPK14. In a rat hemorrhagic shock model, cardiac ROS, Fe2+, MDA, and GSH levels were assessed. Key ferroptotic proteins (SLC7A11/GPX4) in myocardial tissues were examined via western blot. Hub genes, CD44 and MAPK14, expressions were confirmed through immunohistochemistry. Analyzing the GSE64711 dataset revealed 337 differentially expressed genes, including 12 linked to ferroptosis. Enrichment analysis highlighted pathways closely related to ferroptosis. Using Genemania, we found these genes mainly affect ROS metabolism and oxidative stress response. WGCNA identified CD44 and MAPK14 as hub genes. Rat myocardial tissue validation showed significant cardiac damage and elevated ROS and MDA levels, and decreased GSH levels in the hemorrhagic shock model. The ferroptotic pathway SLC7A11/GPX4 was activated, and immunohistochemistry showed a significant increase in the expression levels of CD44 and MAPK14 in the hemorrhagic shock rat model. We demonstrated the presence of tissue ferroptosis in hemorrhagic shock by combining bioinformatics analysis with in vivo experimentation. Specifically, we observed the activation of the SLC7A11/GPX4 ferroptotic pathway. Further, CD44 and MAPK14 were identified as hub genes in hemorrhagic shock. [ABSTRACT FROM AUTHOR]

As a significant method to inhibit metal corrosion by blocking the diffusion of corrosive mediums to the metal surface, the anticorrosion coating with a self-healing function can actively repair a damaged structure and improve the anticorrosion performance to better meet actual needs. In this study, "external aid" and "intrinsic triggering" self-healing coatings have been introduced in detail, including the preparation method, healing mechanism and practical applications. The healing of "external aid" is based on the addition components such as microcapsules containing healing agents and functional nanoparticles, whose ability of self-healing shows the independence with the coating resin. But the finitely additive amount may limit the sustainable use of "external aid" components, and the abundant fillers also change the basic physical properties of the coating. On the contrary, the "intrinsic triggering" resins can form the cover layer in the defects owing to the physical or chemical reactions between the polymer chains, along with the unlimited cycles theoretically. By contrast, the small defects or gaps can be repaired gradually through chain reactions, but the large areas of damage may need the quick release of healing additives in "external aid" coating. In this review, the advances of two kinds of self-healing coatings were analyzed to discuss the advantages and disadvantages of various healing technologies, and the challenges of development and prospects were also forecasted to provide useful ideas. [ABSTRACT FROM AUTHOR]

Introduction: Inflammation is a defensive response of the organism to irritation which is manifested by redness, swelling, heat, pain and dysfunction. The inflammatory response underlies the role of various diseases. Ferroptosis, a unique modality of cell death, driven by iron-dependent lipid peroxidation, is regulated by multifarious cellular metabolic pathways, including redox homeostasis, iron processing and metabolism of lipids, as well as various signaling pathways associated with diseases. A growing body of evidence suggests that ferroptosis is involved in inflammatory response, and targeting ferroptosis has great prospects in preventing and treating inflammatory diseases. Materials and methods: Relevant literatures on ferroptosis, inflammation, inflammatory factors and inflammatory diseases published from January 1, 2010 to now were searched in PubMed database. Conclusion: In this review, we summarize the regulatory mechanisms associated with ferroptosis, discuss the interaction between ferroptosis and inflammation, the role of mitochondria in inflammatory ferroptosis, and the role of targeting ferroptosis in inflammatory diseases. As more and more studies have confirmed the relationship between ferroptosis and inflammation in a wide range of organ damage and degeneration, drug induction and inhibition of ferroptosis has great potential in the treatment of immune and inflammatory diseases. [ABSTRACT FROM AUTHOR]

Ovarian cancer has the highest mortality rate among gynecologic tumors, with a 5-year survival rate of less than 25%. There is an urgent need for early diagnosis and new drugs to reduce the disease burden of ovarian cancer. The aim of this study was to investigate the effectiveness of SLC11A2 as a therapeutic target and marker for ovarian cancer. Expression data of SLC11A2 were obtained from public databases. Then, the biological functions of SLC11A2 were validated in four ovarian cancer cell lines. Finally, we collected ovarian cancer clinical tissues, serum, and plasma exosomes and used immunohistochemistry, Elisa, and liquid chromatography-mass spectrometry (LC–MS) to validate the test efficacy of SLC11A2. The results showed that ovarian cancers with high SLC11A2 mRNA expression had shorter 5-year PFS and MST. Knockdown of SLC11A2 reduced ovarian cancer migration and increased cisplatin-induced apoptosis. Serum SLC11A2 may help improve the detection rate of ovarian cancer. [ABSTRACT FROM AUTHOR]

The behavior characteristics of nano-inhibitors are meaningful to understand the inhibition mechanism and influencing factors of particles in large size. Given the accumulated charge in the outer layer of nanoparticles, the driving force in the electric field will be significantly different from that in traditional inhibitors, and the process of adsorption kinetic will be inevitably changed. In this study, the carbon dots (CDs) were used as the nano-inhibitor for carbon steel in 1 M HCl solution, and the effect of external parallel electric field (PEF) for inhibition performance had been investigated via the various measurements. The results revealed that CDs can effectively inhibit metal corrosion, and the inhibition efficiency reached 90% at only 5 mg/L. Chemisorption and chelation of polar groups in CDs lead to the accumulation, then forming the protective cover layer on metal surface. But the inhibition performance of CDs declined gradually with the increase of electric intensity of PEF, and inhibition efficiency decreased by about 20% according to the results in polarization curve when the electric intensity was in 2 × 105 V/m. The migration direction and aggregation concentration of CDs were affected by the electric field, and there was horizontal force during the adsorption of nanoparticles under PEF, thus the adsorbing performance at the interface weakening with the defective cover layer. [ABSTRACT FROM AUTHOR]

Gastric cancer (GC) is an aggressive malignant tumor of the digestive system, with high morbidity rates. We previously demonstrated that miR-17-5p can modify tumorigenesis in GC. In addition, other studies have shown that circRNAs can regulate GC progression by sponging various miRNAs. However, the association between circRNAs and miR-17-5p in GC has not yet been explored. Hence, this study aimed to explore the possible interactions between various circRNAs and miR-17-5p using a dual-luciferase assay. CCK-8 was used to determine cell viability, and a Transwell assay was used to measure cell invasion and migration. Gene expression was assessed using quantitative reverse transcription PCR (RT-qPCR), and exosomes were identified using transmission electron microscopy (TEM) and nanoparticle tracking analysis (NTA). Annexin V/PI staining was also used to detect cell apoptosis. These investigations collectively revealed that miR-17-5p is a target of the circRNA hsa_circ_0017252 and hsa_circ_0017252 is significantly downregulated in GC tissues. In addition, the overexpression of hsa_circ_0017252 inhibited GC cell migration by sponging of miR-17-5p, and GC cell-secreted exosomal hsa_circ_0017252 effectively inhibited macrophage M2-like polarization, which in turn suppressed GC cell invasion. Notably, exosomes containing hsa_circ_0017252 also suppressed GC tumor growth in vivo. Thus, our data suggest that the overexpression of hsa_circ_0017252 suppresses GC malignancy by sponging miR-17-5p. In addition, exosomal hsa_circ_0017252 excreted from GC cells attenuated GC progression by suppressing macrophage M2-like polarization. These findings improve our basic understanding of GC and open a novel avenue for developing more effective GC treatments. [ABSTRACT FROM AUTHOR]

Checkpoint immunotherapies have been combined with other therapeutic modalities to increase patient response rate and improve therapeutic outcome, which however exacerbates immune-related adverse events and requires to be carefully implemented in a narrowed therapeutic window. Strategies for precisely controlled combinational cancer immunotherapy can tackle this issue but remain lacking. We herein report a catalytical nano-immunocomplex for precise and persistent sono-metabolic checkpoint trimodal cancer therapy, whose full activities are only triggered by sono-irradiation in tumor microenvironment (TME). This nano-immunocomplex comprises three FDA-approved components, wherein checkpoint blockade inhibitor (anti-programmed death-ligand 1 antibody), immunometabolic reprogramming enzyme (adenosine deaminase, ADA), and sonosensitizer (hematoporphyrin) are covalently immobilized into one entity via acid-cleavable and singlet oxygen-activatable linkers. Thus, the activities of the nano-immunocomplex are initially silenced, and only under sono-irradiation in the acidic TME, the sonodynamic, checkpoint blockade, and immunometabolic reprogramming activities are remotely awakened. Due to the enzymatic conversion of adenosine to inosine by ADA, the nano-immunocomplex can reduce levels of intratumoral adenosine and inhibit A2A/A2B adenosine receptors-adenosinergic signaling, leading to efficient activation of immune effector cells and inhibition of immune suppressor cells in vivo. Thus, this study presents a generic and translatable nanoplatform towards precision combinational cancer immunotherapy. Ultrasound-based therapies in combination with immune checkpoint blockade have been shown to improve the efficacy of cancer immunotherapy. Here the authors report the design of a pH-responsive and sono-irradiation activatable nanosystem functionalized with anti-PD-L1 and adenosine deaminase for sono-metabolic cancer immunotherapy. [ABSTRACT FROM AUTHOR]

Immunometabolic intervention has been applied to treat cancer via inhibition of certain enzymes associated with intratumoral metabolism. However, small-molecule inhibitors and genetic modification often suffer from insufficiency and off-target side effects. Proteolysis targeting chimeras (PROTACs) provide an alternative way to modulate protein homeostasis for cancer therapy; however, the always-on bioactivity of existing PROTACs potentially leads to uncontrollable protein degradation at non-target sites, limiting their in vivo therapeutic efficacy. We herein report a semiconducting polymer nano-PROTAC (SPNpro) with phototherapeutic and activatable protein degradation abilities for photo-immunometabolic cancer therapy. SPNpro can remotely generate singlet oxygen (1O2) under NIR photoirradiation to eradicate tumor cells and induce immunogenic cell death (ICD) to enhance tumor immunogenicity. Moreover, the PROTAC function of SPNpro is specifically activated by a cancer biomarker (cathepsin B) to trigger targeted proteolysis of immunosuppressive indoleamine 2,3-dioxygenase (IDO) in the tumor of living mice. The persistent IDO degradation blocks tryptophan (Trp)-catabolism program and promotes the activation of effector T cells. Such a SPNpro-mediated in-situ immunometabolic intervention synergizes immunogenic phototherapy to boost the antitumor T-cell immunity, effectively inhibiting tumor growth and metastasis. Thus, this study provides a polymer platform to advance PROTAC in cancer therapy. Proteolysis targeting chimeras (PROTACs) is an effective alternative to modulate protein homeostasis but can lead to uncontrollable protein degradation and off-target side effects. Here, the authors developed semiconducting polymer nano-PROTACs with phototherapeutic and activatable protein degradation abilities for photo-immunometabolic cancer therapy. [ABSTRACT FROM AUTHOR]

CRISPR/Cas9 system has become a promising gene editing tool for cancer treatment. However, development of a simple and effective nanocarrier to incorporate CRISPR/Cas9 system and chemotherapeutic drugs to concurrently tackle the biological safety and packaging capacity of viral vectors and combine gene editing-chemo for cancer therapy still remains challenges. Herein, a chain-shattering Pt(IV)-backboned polymeric nanoplatform is developed for the delivery of EZH2-targeted CRISPR/Cas9 system (NPCSPt/pEZH2) and synergistic treatment of prostate cancer. The pEZH2/Pt(II) could be effectively triggered to unpack/release from NPCSPt/pEZH2 in a chain-shattering manner in cancer cells. The EZH2 gene disruption efficiency could be achieved up to 32.2% of PC-3 cells in vitro and 21.3% of tumor tissues in vivo, leading to effective suppression of EZH2 protein expression. Moreover, significant H3K27me3 downregulation could occur after EZH2 suppression, resulting in a more permissive chromatin structure that increases the accessibility of released Pt(II) to nuclear DNA for enhanced apoptosis. Taken together, substantial proliferation inhibition of prostate cancer cells and further 85.4% growth repression against subcutaneous xenograft tumor could be achieved. This chain-shattering Pt(IV)-backboned polymeric nanoplatform system not only provides a prospective nanocarrier for CRISPR/Cas9 system delivery, but also broadens the potential of combining gene editing-chemo synergistic cancer therapy. [ABSTRACT FROM AUTHOR]

Chemotherapeutic and radiation therapy have emerged as two most important treatment strategies to treat cancer in clinical practice; however, to improve anticancer efficacy, combination chemotherapy still remains challenge. Dichloroacetate (DCA) could produce significant cytotoxic effects in certain tumor cells through its distinct mechanism. Radiation therapy with fast neutrons (FNT) has high relative biolgical effectiveness compared to other radiotherapeutics. Herein, we reported the combination chemotherapy with FNT for effective tumor growth inhibition with the assistance of a multilayered nanofiber loading DCA and DCA derivatives. We first synthesized a biodegradable polylysine to condense DCA with negative charge, or to conjugate DCA by condensing synthesis, to obtain Ion-DCA and Co-DCA, respectively. DCA, Ion-DCA or Co-DCA was then loaded into fibers to form multilayer drug-loaded mats. Upon adhesion on the surface of subcutaneous and orthotopic liver tumors, the multilayer drug-loaded mats realized a controllable release of DCA, which reversed the Warburg effect and inhibited cancer cell proliferation. Meantime, irradiation of fast neutrons could seriously damage DNA structure. Combination of the controllable release of DCA and FNT resulted in synergistic cell apoptosis in vitro, and the tumor inhibition in vivo. This study thus provides a new approach to integrate chemotherapy and FNT with the assistance of biocompatible nanofiber for synergistic tumor therapy. [ABSTRACT FROM AUTHOR]

Periodontitis is an inflammation characterized by alveolar bone resorption caused by imbalance in bone homeostasis. It is known that autophagy is related to inflammation and bone metabolism. However, whether autophagy inhibitors could be used for periodontitis in animal models remains unknown. We investigated the role of two classical autophagy inhibitors, 3-methyladenine (3-MA) and chloroquine (CQ), on the development of rat experimental periodontitis in terms of the bone loss (micro-CT), the number of inflammatory cells (hematoxylin and eosin staining), and the osteoclastic activity (tartrate-resistant acid phosphatase staining). Expression of autophagy-related genes and nuclear factor kappa B p65 (NF-κB p65) were assessed by immunohistochemistry. Expression of Beclin-1 and microtubule-associated proteins 1A/1B light chain 3 (LC3) were analyzed by Western blot. To further observe the effect of autophagy inhibitors on osteoclasts (OCs) in vitro, bone marrow–derived mononuclear macrophages were used. Together, these findings indicated that topical administration of 3-MA or CQ reduced the infiltration of inflammatory cells and alveolar bone resorption in experimental periodontitis. Furthermore, 3-MA and CQ may attenuate activation of OCs by autophagy. Therefore, 3MA and CQ may have prophylactic and therapeutic potential for inflammation and alveolar bone resorption in periodontitis in the future. [ABSTRACT FROM AUTHOR]

Topographical relief is a key factor that limits population distribution and economic development in mountainous areas. The limitation is especially apparent in the mountain- plain transition zone. Taking the transition zone between the Qinling Mountains and the North China Plain (i.e. the mountainous area in western Henan Province) as an example and based on the 200-m resolution DEM data, we used the mean change-point analysis to determine the optimal statistical unit for topographical relief, and thereafter extracted the relief degree. Taking the 1:100,000 land use data, township population and county-level industrial data, population and economic spatial models were constructed, and 200-m resolution grid population and economic density maps were generated. Afterwards, statistical analysis was carried out to quantitatively reveal the impact of topographical relief on population and economy. In addition, the impacts of other topographical factors were discussed. The results showed the following. (1) The relief degree in western Henan is generally low, where 58.6% of the regional topography does not exceed half the height of a reference mountain (relative elevation ⩽250 m). Spatially, the relief degree is high in the west while low in the east, and high in the middle while low in the north and south. There is a positive correlation between relief degree and elevation, and a much stronger correlation between relief degree and slope. (2) The linear fitting degree between the population and economic validation data and the corresponding simulation data are 0.943 and 0.909, respectively, indicating that the spatialized results can reflect the actual population and economic distribution. (3) The impact of topographical relief on population and economy was stronger than that of other topographical factors. The relief degree showed a good logarithmic fit relationship with population density (0.911) and economic density (0.874). Specifically, 88.65% of the population lives in areas where the topographical relief is ⩽0.5 and 88.03% of the gross regional product was from areas where the relief is ⩽0.3. Compared with the population distribution, the economic development showed an obvious agglomeration trend towards low relief areas. [ABSTRACT FROM AUTHOR]

The present study aimed to elucidate the mechanism of myocardial damage induced by simulated transport stress. Sprague-Dawley rats were subjected to 35 °C and 60 rpm (0.1× g rcf) on a constant temperature shaker. The blood samples were prepared for detection of epinephrine (E), norepinephrine (NE), atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and serum cardiac troponin T (cTNT); myocardium samples were prepared for morphological examination and signaling protein quantitative. The result showed that plasma norepinephrine (NE) and epinephrine (E) concentrations increased in all stressed groups ( P < 0.01). Levels of serum cardiac troponin T (cTNT) were elevated in both the S2d ( P < 0.05) and S3d groups ( P < 0.01). The concentration of plasma BNP was increased significantly in S3d group ( P < 0.05); the difference in ANP was not remarkable. Morphological observation demonstrated obvious microstructure and ultrastructure damage after simulated transport stress. There was also a significant increase in the number of TUNEL-positive cardiomyocytes in stressed hearts. Western blot analysis found that the mitogen-activated protein kinase (MAPK) pathways were activated by strengthening phosphorylation of ASK-1, JNK, P38 and ERK in rat myocardial tissue after simulated transport stress ( P < 0.05, P < 0.01). In addition, the ratio of pro-apoptotic Bax and anti-apoptotic Bcl-2 proteins was increased in stressed rats ( P < 0.01), and the amount of cleaved-caspase3 increased in all stressed rats ( P < 0.01). The expression of cleaved-caspase9 protein was also elevated in S2d and S3d groups ( P < 0.01). Consequently simulated transport stress induced obvious myocardial damage, which may be attributed to the activation of caspase 9-mediated mitochondrial apoptotic pathway and MAPK pathways. [ABSTRACT FROM AUTHOR]

Ferroptosis is the well-known mechanism of septic cardiomyopathy (SCM). Bioinformatics analysis was employed to identify ferroptosis-related SCM differentially expressed genes (DEG). DEGs’ functional enrichment was explored. Weighted gene co-expression network analysis (WGCNA) was employed to form gene clusters. The identified hub genes, signal transducer and activator of transcription 3 (STAT3) and myelocytomatosis (MYC) were further evaluated by generating receiver operator characteristic (ROC) curves and a nomogram prediction model. Additionally, survival rate, cardiac damage markers, and cardiac function and ferroptosis markers were evaluated in septic mouse model. STAT3 and MYC levels were measured in SCM heart tissue via immunohistochemical (IHC) staining, real-time polymerase chain reaction (qPCR) and western blot analysis. Analysis identified 225 DEGs and revealed 22 intersected genes. Of the 7 hub genes, STAT3 and MYC showed enrichment in septic heart tissue and a strong predicative ability based on AUC values. Cardiac damage, iron metabolism, and lipid peroxidation occurred in the SCM model. By experiments, STAT3 and MYC expression was increased in the SCM model. Impairment was reversed with a ferroptosis inhibitor, Fer-1. As conclusion, STAT3 and MYC are related with ferroptosis and may serve as potential SCM predictor indicators.Septic cardiomyopathy (SCM) often leads to high mortality in septic patients, and the diagnostic criteria still remains unclear.Ferroptosis as the pathogenic mechanism of SCM could help predict its progression and clinical outcomes.STAT3 and MYC are related with ferroptosis and may serve as potential SCM predictor biomarkers.Septic cardiomyopathy (SCM) often leads to high mortality in septic patients, and the diagnostic criteria still remains unclear.Ferroptosis as the pathogenic mechanism of SCM could help predict its progression and clinical outcomes.STAT3 and MYC are related with ferroptosis and may serve as potential SCM predictor biomarkers.Key messages: Ferroptosis is the well-known mechanism of septic cardiomyopathy (SCM). Bioinformatics analysis was employed to identify ferroptosis-related SCM differentially expressed genes (DEG). DEGs’ functional enrichment was explored. Weighted gene co-expression network analysis (WGCNA) was employed to form gene clusters. The identified hub genes, signal transducer and activator of transcription 3 (STAT3) and myelocytomatosis (MYC) were further evaluated by generating receiver operator characteristic (ROC) curves and a nomogram prediction model. Additionally, survival rate, cardiac damage markers, and cardiac function and ferroptosis markers were evaluated in septic mouse model. STAT3 and MYC levels were measured in SCM heart tissue via immunohistochemical (IHC) staining, real-time polymerase chain reaction (qPCR) and western blot analysis. Analysis identified 225 DEGs and revealed 22 intersected genes. Of the 7 hub genes, STAT3 and MYC showed enrichment in septic heart tissue and a strong predicative ability based on AUC values. Cardiac damage, iron metabolism, and lipid peroxidation occurred in the SCM model. By experiments, STAT3 and MYC expression was increased in the SCM model. Impairment was reversed with a ferroptosis inhibitor, Fer-1. As conclusion, STAT3 and MYC are related with ferroptosis and may serve as potential SCM predictor indicators.Septic cardiomyopathy (SCM) often leads to high mortality in septic patients, and the diagnostic criteria still remains unclear.Ferroptosis as the pathogenic mechanism of SCM could help predict its progression and clinical outcomes.STAT3 and MYC are related with ferroptosis and may serve as potential SCM predictor biomarkers.Septic cardiomyopathy (SCM) often leads to high mortality in septic patients, and the diagnostic criteria still remains unclear.Ferroptosis as the pathogenic mechanism of SCM could help predict its progression and clinical outcomes.STAT3 and MYC are related with ferroptosis and may serve as potential SCM predictor biomarkers. [ABSTRACT FROM AUTHOR]