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摘要：BackgroundKinesin family member 13B (KIF13B), a crucial motor protein, exerts multiple cellular biological functions. However, the implication of KIF13B in metabolic dysfunction-associated fatty liver disease (MAFLD) has not been explored yet. This study aimed to investigate KIF13B’s role and underlying mechanism in MAFLD and proposes it as a potential pharmacological target.MethodsWe assessed KIF13B expression in MAFLD patients and rodent models. The roles of Kif13b in lipid metabolism and MAFLD were investigated using whole-body Kif13b knockout mice, hepatocyte-specific Kif13b-deficient mice and hamsters exposed to different diets. The underlying mechanisms by which Kif13b governed hepatic lipid homeostasis and MAFLD progression were explored in vitro. Finally, the Kif13b’s impact on atherosclerotic development was studied in the context of MAFLD.ResultsKIF13B expression was reduced in patients and murine models with MAFLD. Rodents with global or liver-specific knockout of the Kif13b gene exhibit spontaneous hepatic steatosis, which is further exacerbated by different overnutrition diets. Overexpression of human KIF13B by lentivirus effectively prevented metabolic dysfunction-associated steatohepatitis (MASH) in methionine-choline-deficient diet (MCD)-fed mice. Furthermore, Kif13b deficiency accelerates atherosclerosis in the context of MAFLD. Mechanistically, Kif13b depletion increases hepatic lipid synthesis and impairs mitochondrial oxidative phosphorylation. Further screening reveals that Kif13b interacts with AMP-activated catalytic subunit alpha 1 (AMPKα1) to regulate the phosphorylation of AMPKα1, governing mitochondrial homeostasis and suppressing sterol regulatory element binding protein 1 (Srebp1)-mediated de novo lipogenesis in the liver.ConclusionThis work establishes a causal relationship between KIF13B deficiency and MAFLD, emphasizing KIF13B as a potential therapeutic target for treating MAFLD.关键词：Kinesin family member 13B;AMP-activated catalytic subunit alpha 1;Mitochondrial homeostasis;Lipid metabolism;Metabolic dysfunction-associated fatty liver disease134|103|0<HTML><网络PDF> <Meta-XML>更新时间：2025-12-13
摘要：BackgroundFibrosis constitutes a significant pathophysiological mechanism in the clinical progression of benign prostatic hyperplasia (BPH) and represents a contributing factor to the ineffectiveness of prevailing pharmacological treatments. Emerging evidence suggests a close association between microbial presence and the development of fibrosis. Nonetheless, the potential involvement of microbes within prostatic tissue in the pathogenesis of BPH and prostatic fibrosis, along with the underlying mechanisms, remains unexplored.MethodsUtilizing immunohistochemistry and microbial sequencing, we analyzed the microbes of prostate tissues from BPH patients with different degrees of prostate fibrosis and found that Salmonella enterica (S. enterica) was enriched in the high degree of prostate fibrosis. We developed prostate cell and animal models infected with the lipopolysaccharide of S. enterica (S.e-LPS) to assess its impact on prostate fibrosis. To elucidate the underlying functional mechanisms, we employed molecular biology techniques, including RNA degradation assays, N6-methyladenosine (m6A) dot blotting, RNA immunoprecipitation, and m6A immunoprecipitation.ResultsMicrobial diversity differed between low- and high-fibrosis groups, with S. enterica showing the highest mean abundance among the four species that differed significantly. S.e-LPS was detected in S. enterica-rich prostate tissue and was found to significantly promote cell proliferation, cell contractility, lipid peroxidation, and the induction of ferroptosis. Animal experiments demonstrated that S.e-LPS infection led to pronounced hyperplasia of the prostatic epithelium, with epithelial thickness increasing to 1.57 times that of the sham group, and collagen fibrosis increasing to 2.84 times that of the sham group, thereby exacerbating prostatic tissue fibrosis in rats. In vitro experiments further revealed that S.e-LPS promoted prostate cell fibrosis by inducing ferroptosis. Mechanistically, it was determined that S.e-LPS regulates ferroptosis via AlkB homolog 5 (ALKBH5)-mediated m6A modification, which affects the stability of glutathione peroxidase 4 (GPX4) mRNA, thereby affecting prostatic fibrosis.ConclusionThe findings of this study suggest that S. enterica promotes prostatic fibrosis through ALKBH5-m6A-GPX4-mediated ferroptosis. This research offers novel insights for the development of new therapeutic targets and personalized strategies for the prevention and treatment of BPH from the perspectives of microbes and epigenetics.关键词：Benign prostatic hyperplasia (BPH);Salmonella enterica (S. enterica);fibrosis;Epigenetic;AlkB homolog 5(ALKBH5)64|23|0<HTML><网络PDF> <Meta-XML>更新时间：2025-12-13
RESEARCH
摘要：Ovarian cancer (OC) remains one of the most lethal gynecological malignancies globally. Despite the implementation of various medical imaging approaches for OC screening, achieving accurate differential diagnosis of ovarian tumors continues to pose significant challenges due to variability in image performance, resulting in a lack of objectivity that relies heavily on the expertise of medical professionals. This challenge can be addressed through the emergence and advancement of radiomics, which enables high-throughput extraction of valuable information from conventional medical images. Furthermore, radiomics can integrate with genomics, a novel approach termed radiogenomics, which allows for a more comprehensive, precise, and personalized assessment of tumor biological features. In this review, we present an extensive overview of the application of radiomics and radiogenomics in diagnosing and pre-dicting ovarian tumors. The findings indicate that artificial intelligence methods based on imaging can accurately dif-ferentiate between benign and malignant ovarian tumors, as well as classify their subtypes. Moreover, these methods are effective in forecasting survival rates, treatment outcomes, metastasis risk, and recurrence for patients with OC. It is anticipated that these advancements will function as decision-support tools for managing OC while contributing to the advancement of precision medicine.关键词：Radiomics;Radiogenomics;Machine learning;Deep learning;ovarian cancer149|52|0<HTML><网络PDF> <Meta-XML>更新时间：2025-12-13
摘要：Sepsis, characterized as life-threatening organ dysfunction resulting from dysregulated host responses to infection, remains a significant challenge in clinical practice. Despite advancements in understanding host-bacterial interac-tions, molecular responses, and therapeutic approaches, the mortality rate associated with sepsis has consistently ranged between 10 and 16%. This elevated mortality highlights critical gaps in our comprehension of sepsis etiology. Traditionally linked to bacterial and fungal pathogens, recent outbreaks of acute viral infections, including Middle East respiratory syndrome coronavirus (MERS-CoV), influenza virus, and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), among other regional epidemics, have underscored the role of viral pathogenesis in sepsis, particu-larly when critically ill patients exhibit classic symptoms indicative of sepsis. However, many cases of viral-induced sepsis are frequently underdiagnosed because standard evaluations typically exclude viral panels. Moreover, these viruses not only activate conventional pattern recognition receptors (PRRs) and retinoic acid-inducible gene-I (RIG-I)-like receptors (RLRs) but also initiate primary antiviral pathways such as cyclic guanosine monophosphate adeno-sine monophosphate (GMP-AMP) synthase (cGAS)-stimulator of interferon genes (STING) signaling and interferon response mechanisms. Such activations lead to cellular stress, metabolic disturbances, and extensive cell damage that exacerbate tissue injury while leading to a spectrum of clinical manifestations. This complexity poses substantial challenges for the clinical management of affected cases. In this review, we elucidate the definition and diagnosis cri-teria for viral sepsis while synthesizing current knowledge regarding its etiology, epidemiology, and pathophysiology, molecular mechanisms involved therein as well as their impact on immune-mediated organ damage. Additionally, we discuss clinical considerations related to both existing therapies and advanced treatment interventions, aiming to enhance the comprehensive understanding surrounding viral sepsis.关键词：Viral sepsis;epidemiology;Definition;Immunopathology;Treatment strategies97|45|0<HTML><网络PDF> <Meta-XML>更新时间：2025-12-13
摘要：Mood disorders include a set of psychiatric manifestations of increasing prevalence in our society, being mainly repre-sented by major depressive disorder (MDD) and bipolar disorder (BD). The etiopathogenesis of mood disorders is extremely complex, with a wide spectrum of biological, psychological, and sociocultural factors being responsible for their appearance and development. In this sense, immune system dysfunction represents a key mechanism in the onset and pathophysiology of mood disorders, worsening mainly the central nervous system (neuroinflammation) and the periphery of the body (sys-temic inflammation). However, these alterations cannot be understood separately, but as part of a complex picture in which different factors and systems interact with each other. Psychoneuroimmunoendocrinology (PNIE) is the area responsible for studying the relationship between these elements and the impact of mind–body integration, placing the immune sys-tem as part of a whole. Thus, the dysfunction of the immune system is capable of influencing and activating different mecha-nisms that promote disruption of the psyche, damage to the nervous system, alterations to the endocrine and metabolic sys-tems, and disruption of the microbiota and intestinal ecosystem, as well as of other organs and, in turn, all these mechanisms are responsible for inducing and enhancing the immune dysfunction. Similarly, the clinical approach to these patients is usu-ally multidisciplinary, and the therapeutic arsenal includes different pharmacological (for example, antidepressants, antipsy-chotics, and lithium) and non-pharmacological (i.e., psychotherapy, lifestyle, and electroconvulsive therapy) treatments. These interventions also modulate the immune system and other elements of the PNIE in these patients, which may be interesting to understand the therapeutic success or failure of these approaches. In this sense, this review aims to delve into the rela-tionship between immune dysfunction and mood disorders and their integration in the complex context of PNIE. Likewise, an attempt will be made to explore the effects on the immune system of different strategies available in the clinical approach to these patients, in order to identify the mechanisms described and their possible uses as biomarkers.关键词：Mood disorders;Immune system;Neuroinflammation;Systemic inflammation;Psychoneuroimmunoendocrinology (PNIE);Pharmacological interventions;Lifestyle medicine64|49|0<HTML><网络PDF> <Meta-XML>更新时间：2025-12-13
摘要：Cancer recurrence, driven by the phenomenon of tumor dormancy, presents a formidable challenge in oncology. Dormant cancer cells have the ability to evade detection and treatment, leading to relapse. This review empha-sizes the urgent need to comprehend tumor dormancy and its implications for cancer recurrence. Despite notable advancements, significant gaps remain in our understanding of the mechanisms underlying dormancy and the lack of reliable biomarkers for predicting relapse. This review provides a comprehensive analysis of the cellular, angiogenic, and immunological aspects of dormancy. It highlights the current therapeutic strategies targeting dormant cells, particularly combination therapies and immunotherapies, which hold promise in preventing relapse. By elucidating these mechanisms and proposing innovative research methodologies, this review aims to deepen our understanding of tumor dormancy, ultimately facilitating the development of more effective strategies for preventing cancer recur-rence and improving patient outcomes.关键词：Tumor dormancy;Cancer recurrence;Signaling pathways;Biomarkers;Therapeutic approaches70|51|0<HTML><网络PDF> <Meta-XML>更新时间：2025-12-13
REVIEW
关键词：Virtual cell;Artificial intelligence;Cancer research;Multi-omics86|27|0<HTML><网络PDF> <Meta-XML>更新时间：2025-12-13
关键词：Idiopathic inflammatory myopathy;Inclusion body myositis (IBM);Interstitial lung disease;Veterans54|38|0<HTML><网络PDF> <Meta-XML>更新时间：2025-12-13
LETTER TO THE EDITOR
- 关键词：Miniaturized percutaneous nephrolithotomy (mPCNL);International Alliance of Urolithiasis (IAU)consensus;Delphi process;Kidney stone surgery47|53|0<HTML><网络PDF> <Meta-XML>更新时间：2025-12-13
COMMENTARY
