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Multiomics profiling reveals the adaptive responses of largemouth bass to high temperature stress.

BACKGROUND: Largemouth bass (Micropterus salmoides) is among the most economically important freshwater fish species. High temperature is a major abiotic stressor, leading to increased mortality and significant economic losses. However, research on the regulatory mechanisms of heat stress response in largemouth bass is limited. This study aims to elucidate the mechanisms of adaptability in largemouth bass during heat stress and subsequent recovery. RESULTS: The morphobiochemical alterations and adaptive mechanisms induced by high water temperature in the gill, brain and liver tissues of large

Crosstalk of thioredoxin system and programmed cell death: from pathophysiology to novel therapy.

The thioredoxin (Trx) system, an integral component of cellular redox regulation, preserves protein dithiol-disulfide equilibrium through its conserved Cys-Gly-Pro-Cys active site and is involved in key cellular functions, including cell proliferation, apoptosis, and signal transduction. In cancer biology, the thioredoxin system plays dual roles: overexpression can suppress oxidative stress and promote tumor growth, whereas dysfunction can trigger programmed cell death (PCD). However, a critical area for future research is to delineate how Trx modulates the intricate networks of PCD, and to id

Совпадение в полном тексте источника
… Therefore, the Trx system is not merely an ancillary component but a fundamental regulator that provides critical pathways for peroxide elimination, and synchronizes the overall antioxidant defense to ensure robust protection against oxidative stress [ 97 ]. …

Genome-Wide Screening and Functional Verification of the Tobacco SGR Family Identify Transcription-Factor-Like NtSGRL as a Negative Regulator of Tomato Yellow Leaf Curl Virus Resistance.

Viral infection often induces chlorosis, a symptom closely associated with chlorophyll (Chl) degradation. STAY-GREEN (SGR) proteins are key regulators of Chl breakdown, but their roles in plant virus resistance remain poorly understood. In this study, we identified six NtSGR family genes in Nicotiana tabacum and functionally characterized NtSGRL1 during tomato yellow leaf curl virus (TYLCV) infection. TYLCV drastically upregulates NtSGRL1 (149-fold at 4 days post-inoculation [dpi] vs. control), suggesting its involvement in the tobacco-TYLCV interaction. Subcellular localization revealed that

Mechanisms of Complement Activation and NETosis Interplay in Early Pregnancy Loss: From Autoimmunity to Thrombogenesis.

Early Pregnancy Loss (EPL) represents a formidable challenge in reproductive medicine. Its complex pathophysiology is primarily characterized by dysregulation of both the immune and coagulation systems. In recent years, abnormal activation of the complement system and neutrophil extracellular trap formation (NETosis) have received increasing scientific attention as key molecular events underlying EPL. This interest is fueled significantly by compelling evidence from non-pregnant models, such as antiphospholipid syndrome (APS) and severe infections (e.g., COVID-19), which demonstrate a pathogen

Ceramide in Type 2 Diabetes and Obesity: Modulation by Nutrients and Dietary Patterns and Opportunities to Prevent and/or Manage Metabolic-Related Conditions.

Ceramides, sphingolipids produced from fatty acids linked to sphingosine and an amide, are structural elements of cellular membranes and lipoproteins. These molecules also retain biological effects in key cellular pathways such as oxidative stress and inflammation, apoptosis, and fibrosis, with a role in the onset and development of many pathophysiological conditions, including obesity, diabetes, and insulin resistance. Increasing evidence suggests that different nutrients and dietary patterns may affect ceramide levels, both negatively (e.g., fructose and the Western diet), whereas others imp

FOXO3a-mediated structural and cellular remodeling in liver tissue: Implications for apoptosis and homeostasis.

FOXO3a, a member of the forkhead box O transcription factor family, has emerged as a pivotal regulator of cellular fate in liver physiology and pathology. Its activity integrates multiple stress signals to orchestrate antioxidant defense, autophagy, and apoptosis, placing it at the intersection of survival and death pathways. Notably, FOXO3a demonstrates a dual role in apoptosis: under certain contexts, it promotes hepatocyte death through activation of pro-apoptotic genes such as Bim and PUMA, contributing to disease progression; conversely, it mitigates oxidative stress and supports cell sur

Ion channels and GPCRs as pharmacological regulators of ferroptosis and pyroptosis in metabolic diseases.

Metabolic diseases, including type 2 diabetes mellitus, obesity, non-alcoholic fatty liver disease, and atherosclerotic cardiovascular disorders, are increasingly recognized as conditions driven not only by metabolic imbalance but also by dysregulated cell death pathways. Beyond apoptosis, ferroptosis and pyroptosis have emerged as pivotal non-apoptotic cell death pathways linking metabolic stress, oxidative injury, and chronic inflammation. Ferroptosis is characterized by iron-dependent lipid peroxidation, while pyroptosis is mediated by inflammasome activation and gasdermin-dependent membran

Targeting Inflammation and Immune Regulation in Chronic Inflammation Associated Cancers.

Chronic inflammation is a fundamental driver of cancer development, linking persistent immune activation to genomic instability, microenvironmental remodeling, and malignant transformation. In inflammation-associated malignancies such as colitis-associated cancer (CAC) and metabolic dysfunction-associated fatty liver disease-related hepatocellular carcinoma (MAFLD-HCC), sustained inflammatory signaling integrates tissue injury with oncogenic pathways to promote tumor initiation and progression. Importantly, these cancers arise through prolonged preneoplastic stages, during which dysregulated i

Exploring Chinese Herbal Medicines for Acute Kidney Injury: Pharmacological Mechanisms and Clinical Potential.

BACKGROUND: Acute kidney injury (AKI) is a serious clinical condition marked by a rapid decline in renal function, leading to high morbidity, mortality, and healthcare burden. Despite advances in supportive care, effective pharmacologic therapies remain lacking, prompting interest in alternative approaches, including Chinese herbal medicines (CHMs). PURPOSE: This review summarizes recent experimental and clinical research on CHMs for AKI, highlighting mechanisms of action, translational challenges, and future directions. METHODS: A narrative review was conducted using PubMed, Web of Science,

Sepsis alters NK cell transcriptional programs for stress, actin remodeling, and intracellular trafficking.

BACKGROUND: Natural killer (NK) cells exert cytotoxicity against transformed and infected cells. In human sepsis, a suppressive NK cell receptor signature and defective effector molecule expression have been described. However, the transcriptional mechanisms underlying this phenotype remain poorly defined. METHODS: We analyzed microarray-based transcriptomic profiles of isolated peripheral NK cells from patients with sepsis, patients with systemic inflammatory response syndrome (SIRS), and presurgical controls. Enrichment analyses of canonical pathways, biological processes, and cellular compa

Near Misses as Signals of System Vulnerability in Thoracic Surgery: A Narrative Review on Quality Improvement and Patient Safety.

Near misses-clinical events that could have resulted in patient harm but did not-are increasingly recognized as critical yet underutilized sources of insight in surgical quality improvement. In thoracic surgery, where procedures are physiologically demanding and care pathways are highly interdependent, near misses frequently precede major complications and expose latent system vulnerabilities rather than isolated technical errors. A structured narrative review methodology was employed, including a targeted literature search of major biomedical databases and thematic synthesis of relevant studi

Identification of susceptibility modules and genes through WGCNA and ceRNA network analysis in neuropathic pain-induced anxiodepression.

Neuropathic pain (NP) is frequently comorbid with anxiety and depression, yet the underlying molecular mechanisms in the brain remain poorly understood, hindering the development of targeted therapies. This study aimed to identify key transcriptional networks and regulatory pathways in the anterior cingulate cortex (ACC) associated with NP-induced anxiodepression. We analyzed transcriptomic data (GSE92718) from the ACC of a mouse model of chronic NP. By comparing differentially expressed genes at a time point manifesting anxiodepressive-like behavior (8-week post-injury) against those with pai

Disrupted glial metabolism and myelin vulnerability in a mouse model of glucose transporter type 1 deficiency syndrome.

Glucose transporter type 1 deficiency syndrome (Glut1DS) is a neurodevelopmental disorder caused by impaired cerebral glucose transport and clinically characterized by absence-type seizures, neurodevelopmental delays, movement disorders, and cognitive deficits. The consequences of chronic cerebral glucose deficiency for glial metabolism and myelin homeostasis remain poorly understood. In this study, we combined metabolic profiling, diffusion MRI, transcriptomic and lipidomic analyses to delineate the metabolic, molecular, and microstructural alterations induced by Glut1 haploinsufficiency in a

Cell-type-specific alkaloid and terpenoid biosynthesis in glandular trichomes: single-cell and spatial transcriptomic perspectives.

Glandular trichomes serve as critical cellular factories for plant secondary metabolism, playing a central role in the biosynthesis, transport, and storage of diverse secondary metabolites. However, traditional macro-scale omics approaches often overlook the cellular heterogeneity within tissues, making it difficult to resolve the specific dynamics of different cell types in glandular trichomes. This limitation has hindered a deeper understanding of secondary metabolic pathways and their regulatory mechanisms. Recent advances in single-cell and spatial omics technologies are now helping to add

Telemedicine for headache disorders in real-world practice: from patient experience to health system impact.

BACKGROUND: Telemedicine has expanded rapidly in neurological care and is increasingly applied to headache management to improve access and continuity of follow-up. However, patient experience and healthcare system impact in real-world practice remain insufficiently explored. OBJECTIVE: The objective of this narrative review is to evaluate clinical effectiveness, patient experience, and healthcare system impact in the management of headache disorders. METHODS: A narrative review of the literature was conducted, including randomized controlled trials, observational studies, real-world evidenc

From epigenetics to metastasis: Multifaceted roles of lncRNAs in gastric cancer.

Gastric cancer (GC) remains one of the leading causes of cancer-related mortality worldwide, largely due to its high metastatic potential and poor prognosis at advanced stages. Epithelial-mesenchymal transition (EMT) is a pivotal biological process that facilitates tumor invasion, dissemination, and therapeutic resistance in GC. In recent years, long non-coding RNAs (lncRNAs) have emerged as critical regulators of gene expression, orchestrating multiple aspects of cancer progression through epigenetic, transcriptional, and post-transcriptional mechanisms. This review provides a comprehensive o

Clinical pathway for patients with suspected heart failure in primary care: Recommendations guided by NT-proBNP testing.

Heart failure (HF) is a highly prevalent condition that contributes significantly to morbidity, mortality, and healthcare burden worldwide. In Portugal, the PORTHOS study estimated that 16.5% of adults aged 50 years and older have HF, underscoring the urgent need for earlier detection and optimized care pathways. N-terminal pro-B-type natriuretic peptide (NT-proBNP) has emerged as a key biomarker for HF screening, diagnosis, and prognosis. The recent reimbursement of NT-proBNP testing in Portuguese primary care represents a critical opportunity to enhance HF detection and management. This posi

In Vivo Multimodal Self-Immolative Prodrug Nanomicelle-Hydrogel Modulate Key Intratumoral and Metastatic Genomic Signaling Pathways in Pancreatic Cancer.

To address the critical challenge of high-lethality pancreatic ductal adenocarcinoma and poor response to conventional chemotherapies, this study introduces a self-immolative micelle encapsulating paclitaxel (PTX) or gemcitabine (GEM), two frontline chemotherapeutic agents. These chemotherapeutic agents present a 2.3-fold reduction for GEM and a 61.7-fold reduction for PTX in IC50 values when conjugated to the micelle system, compared to their free drug counterparts. Through longitudinal bioluminescence imaging, we observed a significant reduction in peritoneal tumor implants versus metastatic

Pellino1-mTOR/S6K1 signaling axis is a key pathogenesis for the development of polycystic kidney disease.

Ubiquitination serves a critical role in regulating both inflammatory responses and kidney injury. Among inherited renal disorders, autosomal dominant polycystic kidney disease (ADPKD) has demonstrated associations with disrupted ubiquitin signaling that exacerbates inflammation and cyst progression. In this study, we demonstrate that the E3 ligase Pellino1 (Peli1) acts as an essential contributor to the pathogenesis of ADPKD amid inflammatory conditions. In individuals with clear cell renal cell carcinoma (ccRCC), Peli1 exhibits markedly elevated expression, and this upregulation is associate

TGF-β3-mediated suppression of SOX2 and OCT4 drives a predominantly non-canonical profile of epithelial-mesenchymal transition during palatal fusion.

Epithelial-mesenchymal transition (EMT) of medial edge epithelial cells is a critical mechanism underlying embryonic palatal fusion, driven by transforming growth factor beta 3 (TGF-β3). However, its regulatory interplay with pluripotency factors (SOX2/OCT4) and reliance on downstream cascades remain poorly understood. This study investigates these networks to elucidate the mechanisms of cellular reprogramming during palatogenesis. Embryonic day 15 C57BL6/J mouse palatal epithelial cells were isolated to eliminate mesenchymal interference. Cells were subjected to recombinant TGF-β3 (1, 3, 10 n