Macrophages are the most important innate immune cells in humans. They are almost ubiquitous in peripheral tissues with a large variety of different mechanical milieus. Therefore, it is not inconceivable that mechanical stimuli have effects on macrophages. Emerging as key molecular detectors of mechanical stress, the function of Piezo channels in macrophages is becoming attractive. In this review, we addressed the architecture, activation mechanisms, biological functions, and pharmacological regulation of the Piezo1 channel and review the research advancements in functions of Piezo1 channels in macrophages and macrophage-mediated inflammatory diseases as well as the potential mechanisms involved.

Immunotherapy has become a successful therapeutic strategy in certain solid tumors and hematological malignancies. However, this efficacy of immunotherapy is impeded by limited success rates. Cellular metabolic reprogramming determines the functionality and viability in both cancer cells and immune cells. Extensive research has unraveled that the limited success of immunotherapy is related to immune evasive metabolic reprogramming in tumor cells and immune cells. As an enzyme that catalyzes the final step of glycolysis, lactate dehydrogenase A (LDHA) has become a major focus of research. Here, we have addressed the structure, localization, and biological features of LDHA. Furthermore, we have discussed the various aspects of epigenetic regulation of LDHA expression, such as histone modification, DNA methylation, N6-methyladenosine (m⁶A) RNA methylation, and transcriptional control by noncoding RNA. With a focus on the extrinsic (tumor cells) and intrinsic (T cells) functions of LDHA in T-cell responses against tumors, in this article, we have reviewed the current status of LDHA inhibitors and their combination with T cell-mediated immunotherapies and postulated different strategies for future therapeutic regimens.

To evaluate the ability of arterial blood lactic acid concentration to predict death within 28 days of admission of patients with severe acute pancreatitis (SAP) in the intensive care unit (ICU).Cl...

The incidence of Gastrointestinal Neoplasms (GI neoplasms) continues to increase globally. Colorectal cancer (CRC), in particular, has emerged as the second leading cause of cancer-related mortality worldwide. Now, Specific pathogenic bacteria, such as Fusobacterium nucleatum (F. nucleatum) and Helicobacter pylori (H. pylori), critically promote tumorigenesis through multiple mechanisms, including the induction of genotoxic damage, host metabolic reprogramming, and remodeling of the tumor immune microenvironment. Notably, a dysbiotic Gut Microbiome (GM) state significantly compromises patient response rates to cancer therapeutics. This review aims to systematically analyze the core molecular mechanism of GM affecting tumor development and explore the precise intervention strategies guided by clinical translation. This systematic review adhered to the PRISMA-2020 guidelines. We conducted a comprehensive literature search in PubMed (2008–2025) using key terms including “Gut Microbiome”, “Gastrointestinal Neoplasms”, “Fecal Microbiota Transplantation (FMT)”, “immunotherapy resistance”, “precision-based interventions”, and “emerging research frontiers”. Preclinical and clinical studies investigating the mechanisms, diagnostic applications, and therapeutic interventions of the GM in GI neoplasms were included. This review systematically elucidates the tripartite mechanisms by which the GM influences the initiation and progression of GI neoplasms. And we innovatively proposed the “Proinflammation-metabolism-Immune framework (Dysbiosis of the GM jointly leads to the occurrence, development and metastasis of GI neoplasms by driving three interrelated processes: chronic inflammation (Proinflammation), reshaping the Metabolism of the host and TME(Metabolism), and inhibiting or altering the host Immune surveillance (Immune))” To deepen the understanding of host-microbe interactions. Based on this framework, we focused on discussing the therapeutic strategy targeting GM and confirmed its significant impact on the efficacy of anti-cancer treatment. Although these strategies have demonstrated clinical potential, current research is still mainly confined to preclinical models and the early clinical trial stage. To address this, we outline future directions: Integrating emerging technologies like multi-omics and artificial intelligence will enable dynamic monitoring and real-time modulation of microbial activity. This integration aims to establish a novel paradigm for microbiome-based personalized precision medicine. This review systematically clarifies that GM is a key target for optimizing the treatment of GI neoplasms. Future research should integrate multi-omics and AI technologies for dynamic microbial monitoring and modulation, paving the way for microbiome-based precision medicine. Overcoming challenges in standardization and clinical translation is essential.

Cancer is a major disease with ever-increasing morbidity and mortality. The metabolites derived from traditional Chinese medicine (TCM) have played a significant role in combating cancers with curative efficacy and unique advantages. Ferroptosis, an iron-dependent programmed death characterized by the accumulation of lipid peroxide, stands out from the conventional forms of cell death, such as apoptosis, pyroptosis, necrosis, and autophagy. Recent evidence has demonstrated the potential of TCM metabolites targeting ferroptosis for cancer therapy. We collected and screened related articles published in or before June 2023 using PubMed, Google Scholar, and Web of Science. The searched keywords in scientific databases were ferroptosis, cancer, tumor, traditional Chinese medicine, botanical drugs, and phytomedicine. Only research related to ferroptosis, the metabolites from TCM, and cancer was considered. In this review, we introduce an overview of the current knowledge regarding the ferroptosis mechanisms and review the research advances on the metabolites of TCM inhibiting cancer by targeting ferroptosis.

Increasing studies showed that miR-200 family (miR-200s) clusters are aberrantly expressed in multiple human cancers, and miR-200s clusters function as tumor suppressor genes by affecting cell proliferation, self-renewal, differentiation, division and apoptosis. Herein, we aimed to investigate the expression and clinical implication of miR-200s clusters in acute myeloid leukemia (AML). RT-qPCR was performed to detect expression of miR-200s clusters in 19 healthy donors, 98 newly diagnosed AML patients, and 35 AML patients achieved complete remission (CR). Expression of miR-200a/200b/429 cluster but not miR-200c/141 cluster was decreased in newly diagnosed AML patients as compared to healthy donors and AML patients achieved CR. Although no significant differences were observed between miR-200s clusters and most of the features, low expression of miR-200s clusters seems to be associated with higher white blood cells especially for miR-200a/200b. Of the five members of miR-200s clusters, low expression of miR-200b/429/200c was found to be associated with lower CR rate. Logistic regression analysis further revealed that low expression of miR-429 acted as an independent risk factor for CR in AML. Based on Kaplan–Meier analysis, low expression of miR-200b/429/200c was associated with shorter OS, whereas miR-200a/141 had a trend. Moreover, multivariate analysis of Cox regression models confirmed the independently prognostic value of miR-200b expression for OS in AML. Expression of miR-200a/200b/429 cluster was frequently down-regulated in AML, and low expression of miR-429 as an independent risk factor for CR, whereas low expression of miR-200b as an independent prognostic biomarker for OS.