Results 111 to 120 of about 6,382 (183)
The establishment and mechanism research in the mice model of actue liver failure [PDF]
背景和目的:急性肝衰竭(acuteliverfailure,ALF)是一个危及生命的严重病理生理状态。它可导致肝脏合成、排泄、解毒、生物转化等功能发生严重障碍或失代偿,出现凝血功能障碍、黄疸以及肝性脑病等主要表现的临床综合征。因其死亡率极高,严重ALF的治疗是当今临床医学中最具有挑战的课题之一。为了有效地治疗ALF,制备与ALF发病经过相同、临床表现类似并可复制的物模型是解决此难题的第一步,而了解各种ALF动物模型的构建机制就显得尤为重要。本课题以氧化偶氮甲烷(azoxymethane,AOM ...
金丽鑫
core
Angiotensin AT2 receptor agonist, compound 21, prevents extracellular matrix degradation, maintains vascular integrity and prevents abdominal aortic aneurysm progression in the rat [PDF]
The effects of angiotensin II Type 2 receptor (AT2R) stimulation on abdominal aortic aneurysm (AAA) formation were investigated in male normotensive Wistar rats. AAA was induced by perfusion of isolated aortic segments with elastase (Anidjar/Dobrin model)
Lange, Christoph
core +1 more source
The functionalized starch modifies the mitochondrial surface and encapsulates resveratrol into the cavity of helices, facilitating a novel mitochondrial transplantation platform (MLSR). Upon internalization in recipient cells, MLSR triggers mitophagy and maintains positive autophagic flux through RIP1/RIP3 pathway inhibition.
Nisha Wang +12 more
wiley +1 more source
RIP1 autophosphorylation is promoted by mitochondrial ROS and is essential for RIP3 recruitment into necrosome [PDF]
韩家淮教授课题组的这项研究揭示了活性氧簇(ROS)通过直接特异地氧化受体相互作用丝氨酸/苏氨酸激酶1(RIP1)上的三个关键的半胱氨酸,进而特异地增强RIP1在S161上的自磷酸化,从而促进坏死小体的形成和程序性细胞坏死的发生。证实了RIP1的激酶活性在程序性细胞坏死中的主要功能是自磷酸化S161,且S161就是人们长期寻找的RIP1上与坏死相关的功能性磷酸化位点。坏死小体的形成是程序性细胞坏死发生的必要复合物,而S161的磷酸化是RIP1有效募集RIP3形成有功能的坏死小体所必需的 ...
Chuan-Qi Zhong +13 more
core +1 more source
PAF Triggered Pyroptotic NETosis Aggravates Myocardial Ischemia/Reperfusion Injury
Platelet activating factor (PAF) secreted by cardiomyocytes during MI/R, drives NETs formation and subsequent NETosis. PAF/NETosis signaling activation is an initiative and causal factor in driving MI/R injury. This study identifies dapagliflozin as a potent NETosis inhibitor, and demonstrates that manipulating PAF‐NETosis signal by dapagliflozin or ...
Jiawei Wu +11 more
wiley +1 more source
TRIM25 acts as a multifunctional hub driving intervertebral disc degeneration under mechanical stress. Mechanical compression significantly upregulates TRIM25 expression, establishing it as a key E3 ubiquitin ligase platform. TRIM25 targets PARG and Ku80 via distinct molecular interfaces, triggering their ubiquitination and degradation.
Zhangrong Cheng +9 more
wiley +1 more source
Holding RIPK1 on the Ubiquitin Leash in TNFR1 Signaling [PDF]
The kinase RIPK1 is an essential signaling node in various innate immune signaling pathways being most extensively studied in the TNFR1 signaling pathway.
Darding, M, Peltzer, N, Walczak, H
core
GSDMD membrane pore formation constitutes the mechanism of pyroptotic cell death [PDF]
Pyroptosis is a lytic type of cell death that is initiated by inflammatory caspases. These caspases are activated within multi-protein inflammasome complexes that assemble in response to pathogens and endogenous danger signals.
Broz, Petr +9 more
core +1 more source
The schematic diagram illustrates the roles of novel immune checkpoints, immunomodulatory factors, cell death and multimodal technologies in cancer immunotherapy. Abstract Cancer immunotherapy has redefined cancer treatment. However, the molecular and cellular basis of immune evasion and therapeutic resistance remains incompletely understood.
Fangquan Chen +7 more
wiley +1 more source
Poly-ubiquitination in TNFR1-mediated necroptosis [PDF]
Tumor necrosis factor (TNF) is a master pro-inflammatory cytokine, and inappropriate TNF signaling is implicated in the pathology of many inflammatory diseases.
Henning Walczak +3 more
core +3 more sources

