Результаты поиска

Инфекция аденовируса 4 серотипа подталкивает уровни кальция к эндоплазмическому ретикулумному стрессу, чтобы стимулировать вирусное воспроизведение в клетках LMH.

Синдром гепатита-гидроперикардия (HHS), вызываемый серотипом 4 птицы (FAdV-4), является острым и крайне смертельным заболеванием, представляющим серьезную угрозу для мировой птицеводческой промышленности. Ионы кальция служат важными вторыми посыльными, которые регулируют несколько этапов вирусного жизненного цикла, включая вход, воспроизведение и сборку. Однако вопрос о том, использует ли FADV-4 внутриклеточный сигнал кальция для облегчения его собственного воспроизведения, остается в значительной степени неисследованным. Здесь мы показываем, что инфекция FADV-4 значительно повышает уровень вн

Совпадение в аннотации оригинала
Hepatitis-hydropericardium syndrome (HHS), caused by fowl adenovirus serotype 4 (FAdV-4), is an acute and highly fatal disease that poses a … vels in LMH cells in a time- and dose-dependent manner. Mechanistically, FAdV-4 induces endoplasmic reticulum (ER) stress, which in turn upregulates the expression of STIM1 and ORAI1 and promotes the translocation of STIM1 to the plasma membrane, thereby activating the store-operated calcium entry (SOCE) channel and driving sustained intracellular calcium e …

Yinchen-Gancao decoction ameliorated NASH in mice by reducing hepatic lipid accumulation, inhibiting hepatic inflammatory and endoplasmic reticulum stress.

ETHNOPHARMACOLOGICAL RELEVANCE: Nonalcoholic steatohepatitis (NASH) poses significant health risks; however, effective treatment options rem … er, these effects were absent in the Fxr-/- mice. YG inhibited hepatic inflammation and endoplasmic reticulum stress (ERS) in both WT and Fxr-/- mice. CONCLUSION: Our study supported the use of YG as a promising therapeutic agent to attenuate NASH. Its mechanism of action involved the reduction of hepatic lipid accumulation (FXR-dependent) and the inhibiti …

7-Ketodeoxycholic Acid Promotes Colonic Mucosal Healing by Inducing Calcium Release from Endoplasmic Reticulum via the TGR5-IP3R Pathway.

Defective healing of injured mucosa is a hallmark of many pathological conditions, such as ulcerative colitis (UC). Wound healing is a pivot … ving intestinal epithelial cell migration through induction of calcium release from the endoplasmic reticulum via targeting the TGR5-IP3R axis. Amidst the array of endogenous metabolites potentially active in progression of UC, 7-KDCA stands out as the preeminent facilitator in the healing of colonic mucosa. This finding may hold clinical significance for t …

LncRNA ZFAS1 Combined with SRSF1 Regulate CNPY2 Expression and Leads to Microglia Endoplasmic Reticulum Stress-Induced Spinal Cord Injury.

Spinal cord injury (SCI) has a high mortality and disability rate. Endoplasmic reticulum (ER) stress induces neuronal apoptosis and participates in the regulation of SCI. LncRNA ZFAS1 can participate in the regulation of SCI by influencing ER stress; however, its mechanism is worth further exploring. The molecular mechanism of lncRNA ZFAS1 regulating spinal cord injury was evaluated by in vitro and in vivo experiments. We established an SCI model in vitro by inducing mouse microglia (BV-2) with LPS. The regulation of SCI was verified by transfection of shRNA knockdown lncRNA ZFAS1 and CNPY2. T…

18β-Glycyrrhetinic Acid Regulates Endoplasmic Reticulum Stress and Autophagy Dysregulation in the MPTP/p-Induced Model of Parkinson Disease.

Parkinson disease (PD) is marked by a significant reduction in dopaminergic neurons in the substantia nigra pars compacta region of the brain. This neuronal loss is accompanied by aggregation of the α-synuclein protein, persistent endoplasmic reticulum (ER) stress, and disruption in the autophagy process. 18β-Glycyrrhetinic acid (18βGA), an oleanolic acid-type triterpenoid, has been shown to exhibit anti-inflammatory properties and neuroprotective effects. This study is the first to explore the potential neuroprotective effects of 18βGA in a chronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine…

AATF alleviates cerebral ischemia-reperfusion injury by suppressing endoplasmic reticulum stress-induced ferroptosis through upregulating the PI3K/Akt pathway.

OBJECTIVE: The study aimed to investigate the role of apoptosis-antagonizing transcription factor (AATF) in regulating endoplasmic reticulum (ER) stress-ferroptosis interaction and its neuroprotective mechanism in cerebral ischemia-reperfusion injury (CIRI). METHODS: Two models were used: oxygen-glucose deprivation/reperfusion (OGD/R)-induced hippocampal neuron cells and transient middle cerebral artery occlusion/reperfusion (tMCAO/R)-induced rats. AATF overexpression and knockdown were respectively performed to assess its impact on neuronal injury. Ferroptosis biomarkers - glutathione peroxi…

Protective functions of liver X receptor α on calcified aortic valve: involvement of regulating endoplasmic reticulum-mediated osteogenic differentiation.

AIMS: Effective therapeutic drugs for calcific aortic valve disease (CAVD) are lacking, although its incidence has been increasing over the … ion both in vitro and in vivo. We showed that LXRα suppressed the protein kinase R-like endoplasmic reticulum kinase/eukaryotic initiation factor 2/activating transcription factor 4 pathway, which controls endoplasmic reticulum stress (ERS) and promotes osteogenic differentiation, thereby slowing the course of CAVD. CONCLUSION: Our research offers fresh pe …

Irisin and liraglutide combination therapy mitigates myocardial reperfusion injury in obese rats: Role of endoplasmic reticulum stress and apoptosis.

BACKGROUND: Obesity has become a global health concern, with its prevalence steadily rising across populations. Apart from its well-known association with various metabolic disorders, obesity has also been linked to an increased risk of cardiovascular diseases, including myocardial ischemia-reperfusion (IR) injury. This study aimed to assess how irisin and liraglutide, when used together, impact endoplasmic reticulum (ER) stress-induced apoptosis and PI3K/AKT signaling in obese rats after cardiac IR injury. METHODS: Thirty-six male Sprague-Dawley rats (200-230 g) were fed either a low-fat or …

Schizandrin A promotes apoptosis in prostate cancer by inducing ROS-mediated endoplasmic reticulum stress and JNK MAPK signaling activation.

BACKGROUND: Prostate cancer (PCa) is the most common malignant tumor in males with limited therapies. Schizandrin A (SchA) is a biologically … rest at G2/M and apoptosis in PCa cells. Additionally, SchA enhanced ROS generation and endoplasmic reticulum stress and activated JNK signaling to induce PCa apoptosis. Furthermore, SchA suppressed tumor growth in vivo. CONCLUSION: SchA induces cell cycle arrest and apoptosis in PCa cells by activating ROS-mediated ER stress and JNK MAPK signaling.

Andrographolide ameliorates sepsis-induced acute liver injury by attenuating endoplasmic reticulum stress through the FKBP1A-mediated NOTCH1/AK2 pathway.

Andrographolide (AP) has been shown to possess anti-inflammatory activities. In this study, the impact of AP in sepsis-induced acute liver i … P1A. NOTCH1 promoted AK2 transcription in liver parenchymal cells, and FKBP1A inhibited endoplasmic reticulum (ER) stress by impairing NOTCH1/AK2 signaling. Restoration of NOTCH1 significantly reversed the hepatoprotective effect of AP in ALI mice and LPS-induced liver parenchymal cell injury by activating the ER stress pathway. Therefore, AP-promoted FKBP1 …

A novel GCGR/GLP-1R dual-agonist TB001 ameliorates kidney fibrosis via inhibiting PERK-mediated endoplasmic reticulum stress pathway.

BACKGROUND: Chronic kidney disease (CKD) affects over one million individuals worldwide and remain a critical economic and healthcare burden. Renal fibrosis is the hallmark of CKD. Previous reports showed that GLP-1R agonists could help prevent kidney fibrosis in diabetic patients. In this study, we aimed to determine the efficacy of a novel GLP-1R and GCGR co-agonist, TB001 in the development of renal fibrosis using both in vitro and in vivo models. METHODS: Unilateral ureteral obstruction (UUO) surgery was performed on adult B6 mice to establish a mouse model of kidney fibrosis. Mice that u

Dimethyl fumarate ameliorated pyroptosis in contrast-induced acute renal injury by regulating endoplasmic reticulum stress and JAK2-STAT3 pathway.

BACKGROUND: Inflammation and oxidative stress are important pathological processes of contrast-induced acute renal injury (CIAKI). This study explored whether DMF had therapeutic effects and investigated the underlying mechanism in CIAKI. METHODS: A CIAKI animal model was established in C57BL/6J mice with iohexol, and DMF was used as an intervention. In vitro, HK-2 cells were treated with iohexol and DMF. RNA-seq analysis was performed on the renal tissue of the mice. Protein-protein interaction (PPI), and enrichment analysis were subsequently conducted. In addition, endoplasmic reticulum str…

Metformin Ameliorates Early Brain Injury After Subarachnoid Hemorrhage Via Improving Endoplasmic Reticulum Stress and Mitochondrial Stress-Mediated Ca2+ Imbalance.

Subarachnoid hemorrhage (SAH) is a destructive subtype of stroke characterized by a high mortality and morbidity rate (45-50%) and a poor neurologic prognosis, encompassing both neurological and psychiatric impairments. It will be more imperative to explore new therapeutic strategies for early brain injury (EBI) to enhance the prognosis of patients with SAH. First, we investigated the role of endoplasmic reticulum stress (ERS) and mitochondrial stress (MS) in mediating the IP3R1-GRP75-VDAC1 Ca2⁺ channeling complex within the first 72 h following SAH in mice. Neurological function was assessed …

JAK1/2 Inhibitors Alleviate the Damage of Intercellular Adhesion by Reducing Endoplasmic Reticulum Stress-Induced Apoptosis in Pemphigus Vulgaris.

Pemphigus vulgaris (PV), a severe autoimmune disease with high morbidity and mortality, necessitates innovative therapies to improve outcome … r, significantly reduced keratinocyte apoptosis, enhanced cell adhesion, and alleviated endoplasmic reticulum (ER) stress. Additionally, Ruxolitinib mitigated tunicamycin-induced ER stress and apoptosis in HaCaT cells. These findings establish a crucial role for JAK1/2 in PV pathogenesis, demonstrating that their inhibition alleviates ER stress, reduces apo …

Bioinformatics identification of key genes correlating NOD1 and Endoplasmic Reticulum stress in Hepatitis B virus-induced acute liver failure.

Endoplasmic reticulum stress (ERS) has been implicated in a range of biological processes, yet its specific involvement in Hepatitis B virus-associated acute liver failure (HBV-ALF) remains poorly understood. This study aimed to identify key ERS-related genes (ERGs) and elucidate their underlying mechanisms in HBV-ALF. Publicly available HBV-ALF-related datasets (GSE38941, GSE62029) and ERGs were analyzed. Intersection genes were determined by overlapping differentially expressed genes from both datasets with ERGs, and genes showing strong correlation with NOD1 were selected as candidates. The…

Effect of 2,5-hexanedione on rat ovarian granulosa cell apoptosis involves endoplasmic reticulum stress-dependent m-TOR signaling pathway.

Occupational exposure to N-hexane/2,5-hexanedione (2,5-HD) was found to adversely affect reproductive functions in females. However, there are few studies regarding the mechanisms underlying reproductive system damage initiated by 2,5-HD. Several studies demonstrated that 2,5-HD exerts hormonal dysfunctions in females by promoting apoptosis using rat ovarian granulosa cells (GCs) as a model. The endoplasmic reticulum (ER) plays a key role in cellular processes such as protein folding and modification, Ca2+ storage, and lipid synthesis, which are known to involve the activation of stress (ERS)-…

Steroidogenesis Upregulation through Mitochondria-Associated Endoplasmic Reticulum Membranes and Mitochondrial Dynamics in Rat Testes: The Role of D-Aspartate.

Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs) mediate the communication between the Endoplasmic Reticulum (ER) and the mitochondria, playing a fundamental role in steroidogenesis. This study aimed to understand how D-aspartate (D-Asp), a well-known stimulator of testosterone biosynthesis and spermatogenesis, affects the mechanism of steroidogenesis in rat testes. Our results suggested that D-Asp exerts this function through MAMs, affecting lipid trafficking, calcium signaling, ER stress, and mitochondrial dynamics. After 15 days of oral administration of D-Asp to rats, there w…

Genome-wide CRISPR/Cas9 screen shows that loss of GET4 increases mitochondria-endoplasmic reticulum contact sites and is neuroprotective.

Organelles form membrane contact sites between each other, allowing for the transfer of molecules and signals. Mitochondria-endoplasmic reticulum (ER) contact sites (MERCS) are cellular subdomains characterized by close apposition of mitochondria and ER membranes. They have been implicated in many diseases, including neurodegenerative, metabolic, and cardiac diseases. Although MERCS have been extensively studied, much remains to be explored. To uncover novel regulators of MERCS, we conducted a genome-wide, flow cytometry-based screen using an engineered MERCS reporter cell line. We found 410 g…

Mitochondria-associated endoplasmic reticulum membranes involve in oxidative stress-induced intestinal barrier injury and mitochondrial dysfunction under diquat exposing.

Many factors induced by environmental toxicants have made oxidative stress a risk factor for the intestinal barrier injury and growth restriction, which is serious health threat for human and livestock and induces significant economic loss. It is well-known that diquat-induced oxidative stress is implicated in the intestinal barrier injury. Although some studies have shown that mitochondria are the primary target organelle of diquat, the underlying mechanism remains incompletely understood. Recently, mitochondria-associated endoplasmic reticulum membranes (MAMs) have aroused increasing concern…

MicroRNA-5572 Is Associated with Endoplasmic Reticulum Stress Responses in Low Zinc Treated and SOD1 G85R-Transfected HEK293 Cells.

Amyotrophic lateral sclerosis (ALS) is a fetal neurodegenerative disease. The mechanism of sporadic ALS onset remains unclarified in detail. … ctor. The miR-5572 level was increased by low-zinc condition accompanied by increase of endoplasmic reticulum (ER) stress. In addition, increase of miR-5572 enhanced the cellular toxicity induced by low-zinc treatment. The expression of miR-5572 was also increased, which was accompanied by an increase of ER stress markers associated with SOD1 aggregation fo …