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| 1 | Diabetic nephropathy and inflammation显示文摘Diabetic nephropathy(DN) is the leading cause of end-stage renal failure worldwide. Besides, diabetic nephropathy is associated with cardiovascular disease, and increases mortality of diabetic patients. Several factors are involved in the pathophysiology of DN, including metabolic and hemodynamic alterations, oxidative stress, and activation of the renin-angiotensin system. In recent years, new pathways involved in the development and progression of diabetic kidney disease have been elucidated; accumulated data have emphasized the critical role of inflammation in the pathogenesis of diabetic nephropathy. Expression of cell adhesion molecules, growth factors, chemokines and pro-inflammatory cytokines are increased in the renal tissues of diabetic patients, and serum and urinary levels of cytokines and cell adhesion molecules, correlated with albuminuria. In this paper we review the role of inflammation in the development of diabetic nephropathy, discussing some of the major inflammatory cytokines involved in the pathogenesis of diabetic nephropathy, including the role of adipokines, and take part in other mediators of inflammation, as adhesion molecules. | Montserrat B Duran-Salgado Alberto F Rubio-Guerra | 2014 | World Journal of Diabetes2014，5，3： | 169 |
| 2 | Sodium oligomannate therapeutically remodels gut microbiota and suppresses gut bacterial amino acids-shaped neuroinflammation to inhibit Alzheimer's disease progression显示文摘Recently,increasing evidence has suggested the association between gut dysbiosis and Alzheimer's disease(AD)progression,yet the role of gut microbiota in AD pathogenesis remains obscure.Herein,we provide a potential mechanistic link between gut microbiota dysbiosis and neuroinflammation in AD progression.Using AD mouse models,we discovered that,during AD progression,the alteration of gut microbiota composition leads to the peripheral accumulation of phenylalanine and isoleucine,which stimulates the differentiation and proliferation of pro-inflammatory T helper 1(Thl)cells.The brain-infiltrated peripheral Th1 immune cells are associated with the Ml microglia aaivation,contributing to AD-associated neuroinflammation.Importantly,the elevation of phenylalanine and isoleucine concentrations and the increase of Th1 cell frequency in the blood were also observed in two small independent cohorts of patients with mild cognitive impairment(MCI)due to AD.Furthermore,GV-971,a sodium oligomannate that has demonstrated solid and consistent cognition improvement in a phase 3 clinical trial in China,suppresses gut dysbiosis and the associated phenylalanine/isoleucine accumulation,harnesses neuroinflammation and reverses the cognition impairment.Together,our findings highlight the role of gut dysbiosis-promoted neuroinflammation in AD progression and suggest a novel strategy for AD therapy by remodelling the gut microbiota. | Xinyi Wang Guangqiang Sun Teng Feng Jing Zhang Xun Huang Tao Wang Zuoquan Xie Xingkun Chu Jun Yang Huan Wang Shuaishuai Chang Yanxue Gong Lingfei Ruan Guanqun Zhang Siyuan Yan Wen Lian Chen Du Dabing Yang Qingli Zhang Feifei Lin Jia Liu Haiyan Zhang Changrong Ge Shifu Xiao Jian Ding Meiyu Geng | 2019 | Cell Research2019，29，10： | 192 |
| 3 | Autophagy and inflammation in ischemic stroke显示文摘Appropriate autophagy has protective effects on ischemic nerve tissue,while excessive autophagy may cause cell death.The inflammatory response plays an important role in the survival of nerve cells and the recovery of neural tissue after ischemia.Many studies have found an interaction between autophagy and inflammation in the pathogenesis of ischemic stroke.This study outlines recent advances regarding the role of autophagy in the post-stroke inflammatory response as follows.(1)Autophagy inhibits inflammatory responses caused by ischemic stimulation through mTOR,the AMPK pathway,and inhibition of inflammasome activation.(2)Activation of inflammation triggers the formation of autophagosomes,and the upregulation of autophagy levels is marked by a significant increase in the autophagy-forming markers LC3-II and Beclin-1.Lipopolysaccharide stimulates microglia and inhibits ULK1 activity by direct phosphorylation of p38 MAPK,reducing the flux and autophagy level,thereby inducing inflammatory activity.(3)By blocking the activation of autophagy,the activation of inflammasomes can alleviate cerebral ischemic injury.Autophagy can also regulate the phenotypic alternation of microglia through the nuclear factor-κB pathway,which is beneficial to the recovery of neural tissue after ischemia.Studies have shown that some drugs such as resveratrol can exert neuroprotective effects by regulating the autophagy-inflammatory pathway.These studies suggest that the autophagy-inflammatory pathway may provide a new direction for the treatment of ischemic stroke. | Yun Mo Yin-Yi Sun Kang-Yong Liu | 2020 | Neural Regeneration Research2020，15，8： | 90 |
| 4 | Ferroptosis:molecular mechanisms and health implications显示文摘Cell death can be executed through different subroutines.Since the description of ferroptosis as an iron-dependent form of nonapoptotic cell death in 2012,there has been mounting interest in the process and function of ferroptosis.Ferroptosis can occur through two major pathways,the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway.Ferroptosis is caused by a redox imbalance between the production of oxidants and antioxidants,which is driven by the abnormal expression and activity of multiple redox-active enzymes that produce or detoxify free radicals and lipid oxidation products.Accordingly,ferroptosis is precisely regulated at multiple levels,including epigenetic,transcriptional,posttranscriptional and posttranslational layers.The transcription factor NFE2L2 plays a central role in upregulating anti-ferroptotic defense,whereas selective autophagy may promote ferroptotic death.Here,we review current knowledge on the integrated molecular machinery of ferroptosis and describe how dysregulated ferroptosis is involved in cancer,neurodegeneration,tissue injury,inflammation,and infection. | Daolin Tang Xin Chen Rui Kang Guido Kroemer | 2021 | Cell Research2021，31，2： | 182 |
| 5 | Necroptosis, pyroptosis and apoptosis: an intricate game of cell death显示文摘Cell death is a fundamental physiological process in all living organisms.Its roles extend from embryonic development,organ maintenance,and aging to the coordination of immune responses and autoimmunity.In recent years,our understanding of the mechanisms orchestrating cellular death and its consequences on immunity and homeostasis has increased substantially.Different modalities of what has become known as‘programmed cell death’have been described,and some key players in these processes have been identified.We have learned more about the intricacies that fine tune the activity of common players and ultimately shape the different types of cell death.These studies have highlighted the complex mechanisms tipping the balance between different cell fates.Here,we summarize the latest discoveries in the three most well understood modalities of cell death,namely,apoptosis,necroptosis,and pyroptosis,highlighting common and unique pathways and their effect on the surrounding cells and the organism as a whole. | Damien Bertheloot Eicke Latz Bernardo S.Franklin | 2021 | Cellular & Molecular Immunology2021，18，5： | 84 |
| 6 | Inflammation, oxidative stress and renin angiotensin system in atherosclerosis显示文摘Atherosclerosis is a chronic inflammatory disease associated with cardiovascular dysfunction including myocardial infarction, unstable angina, sudden cardiac death, stroke and peripheral thromboses. It has been predicted that atherosclerosis will be the primary cause of death in the world by 2020. Atherogenesis is initiated by endothelial injury due to oxidative stress associated with cardiovascular risk factors including diabetes mellitus, hypertension, cigarette smoking, dyslipidemia, obesity, and metabolic syndrome. The impairment of the endothelium associated with cardiovascular risk factors creates an imbalance between vasodilating and vasoconstricting factors, in particular, an increase in angiotensin Ⅱ(Ang Ⅱ) and a decrease in nitric oxide. The renin-angiotensin system(RAS), and its primary mediator Ang Ⅱ, also have a direct influence on the progression of the atherosclerotic process via effects on endothelial function, inflammation, fibrinolytic balance, and plaque stability. Anti-inflammatory agents [statins, secretory phospholipase A2 inhibitor, lipoprotein-associated phospholipase A2 inhibitor, 5-lipoxygenase activating protein, chemokine motif ligand-2, C-C chemokine motif receptor 2 pathway inhibitors, methotrexate, IL-1 pathway inhibitor and RAS inhibitors(angiotensin-converting enzyme inhibitors)], Ang Ⅱ receptor blockers and ranin inhibitors may slow inflammatory processes and disease progression. Several studies in human using anti-inflammatory agents and RAS inhibitors revealed vascular benefits and reduced progression of coronary atherosclerosis in patients with stable angina pectoris; decreased vascular inflammatory markers, improved common carotid intima-media thickness and plaque volume in patients with diagnosed atherosclerosis. Recent preclinical studies have demonstrated therapeutic efficacy of vitamin D analogs paricalcitol in Apo E-deficient atherosclerotic mice. | Kazim Husain Wilfredo Hernandez Rais A Ansari Leon Ferder | 2015 | World Journal of Biological Chemistry2015，6，3： | 84 |
| 7 | Modulation of postoperative immune and inflammatory response by immune-enhancing enteral diet in gastrointestinal cancer patients显示文摘AIM To evaluate if the administration of anenteral diet supplemented with glutamine,arginine and ω-3-fatty acids modulatesinflammatory and immune responses aftersurgery.METHODS A prospective randomized double-blind, clinical trial was performed. Forty-eightpatients with gastrointestinal cancer wererandomized into two groups, one group wasgiven an isocaloric and isonitrogenous standarddiet and the other was fed with the supplementeddiet with glutamine, arginine and ωo-3-fattyacids. Feedings were started within 48 hoursafter operation, and continued until day 8. Allvariables were measured before operation andon postoperative day 1 and 8. Immune responseswere determined by phagocytosis ability,respiratory burst of polymorphonuclear cells,total lymphocytes lymphocyte subsets, nitricoxide, cytokines concentration, andinflammatory responses by plasma levels of C-reactive protein, prostaglandin E2 level.RESULTS Tolerance of both formula diets wasexcellent. There were siagnificant differences inthe immunological and inflammatory responsesbetween the two groups. In supplementedgroup, phagocytosis and respiratory burst aftersurgery was higher and C-reactive protein levelwas lower (P<0.01) than in the standard group.The supplemented group had higher levels ofnitric oxide, total Iymphocytes, T lymphocytes,T-helper cells, and NK cells. Postoperativelevels of IL-6 and TNF-α were lower in thesupplemented group ( P < 0.05).CONCLUSION It was clearly established in thistrial that early postoperative enteral feeding issafe in patients who have undergone majoroperations for gastrointestinal cancer.Supplementation of enteral nutrition withglutamine, arginine, and ω-3 fatty acidspositively modulated postsurgicalimmunosuppressive and inflammatoryresponses. | Guo Hao Wu Yan Wei Zhang Zhao Han Wu Department of General Surgery.zhongshan Hospital,ShangHai Medical University.ShangHai 200032.China | 2001 | World Journal of Gastroenterology2001，7，3： | 67 |
| 8 | Progress on the pharmacological research of puerarin: a review显示文摘Contemporary pharmacological research has demonstrated that puerarin, the most important phytoestrogen extracted from Pueraria lobata(Willd.) Ohwi, has protecting functions on the cardiovascular system, nervous system, osteoporosis, liver injury, and inflammation in vivo and in vitro. Most of these research studies focused on inhibiting oxidative stress and apoptosis through regulating various bioactivators and signal pathways. Among these, superoxide dismutase(SOD), endothelial nitric oxide synthase(eNOS) and malondialdehyde(MDA), and PI3K/Akt, MAPK, and NF-κB are of great importance. The data cited in this review were mainly obtained from articles listed in PubMed and Elsevier SDOL published from 1959 to 2013, and the search term used was 'puerarin'. | WEI Shu-Yong CHEN Yi XU Xiao-Yu | 2014 | Chinese Journal of Natural Medicines2014，12，6： | 62 |
| 9 | Interaction between the gut microbiome and mucosal immune system显示文摘The gut microbiota, the largest symbiotic ecosystem with the host, has been shown to play important roles in maintaining intestinal homeostasis. Dysbiosis of the gut microbiome is caused by the imbalance between the commensal and pathogenic microbiomes. The commensal microbiome regulates the maturation of the mucosal immune system, while the pathogenic microbiome causes immunity dysfunction, resulting in disease development.The gut mucosal immune system, which consists of lymph nodes, lamina propria and epithelial cells, constitutes a protective barrier for the integrity of the intestinal tract. The composition of the gut microbiota is under the surveillance of the normal mucosal immune system. Inflammation, which is caused by abnormal immune responses,influences the balance of the gut microbiome, resulting in intestinal diseases. In this review, we briefly outlined the interaction between the gut microbiota and the immune system and provided a reference for future studies. | Na Shi Na Li Xinwang Duan Haitao Niu | 2017 | Military Medical Research2017，4，3： | 65 |
| 10 | Dual Functions of Microglia in Ischemic Stroke显示文摘Ischemic stroke is a leading cause of morbidity and mortality worldwide. Resident microglia are the principal immune cells of the brain, and the first to respond to the pathophysiological changes induced by ischemic stroke. Traditionally, it has been thought that microglial activation is deleterious in ischemic stroke, and therapies to suppress it have been intensively explored. However,increasing evidence suggests that microglial activation is also critical for neurogenesis, angiogenesis, and synaptic remodeling, thereby promoting functional recovery after cerebral ischemia. Here, we comprehensively review the dual role of microglia during the different phases of ischemic stroke, and the possible mechanisms controlling the post-ischemic activity of microglia. In addition, we discuss the dynamic interactions between microglia and other cells, such as neurons, astrocytes, oligodendrocytes,and endothelial cells within the brain parenchyma and the neurovascular unit. | Chuan Qin Luo-Qi Zhou Xiao-Tong Ma Zi-Wei Hu Sheng Yang Man Chen Dale B. Bosco Long-Jun Wu Dai-Shi Tian | 2019 | Neuroscience Bulletin2019，35，5： | 64 |
| 11 | Pathophysiological 角色和在糖尿病的 nephropathy 的发炎的治疗学的含意显示文摘 Diabetes mellitus and its complications are becoming one of the most important health problems in the world. Diabetic nephropathy is now the main cause of end-stage renal disease. The mechanisms leading tothe development and progression of renal injury are not well known. Therefore, it is very important to f ind new pathogenic pathways to provide opportunities for early diagnosis and targets for novel treatments. At the present time, we know that activation of innate immunity with development of a chronic low grade inflammatory response is a recognized factor in the pathogenesis of diabetic nephropathy. Numerous experimental and clinical studies have shown the participation of different inflammatory molecules and pathways in the pathophysiology of this complication. | Desirée Luis-Rodríguez Alberto Martínez-Castelao José Luis Górriz Fernando de lvaro Juan F Navarro-González | 2012 | World Journal of Diabetes2012，3，1： | 55 |
| 12 | Aetiology of idiopathic granulomatous mastitis显示文摘Idiopathic granulomatous mastitis is a rare chronic inflammatory lesion of the breast that can clinically and radiographically mimic breast carcinoma. The most common clinical presentation is an unilateral, discrete breast mass, nipple retraction and even a sinus formation often associated with an inflammation of the overlying skin. The etiology of idiopathic granulomatous mastitis is still obscure. Its treatment remains controversial. The cause may be the autoimmune process, infection, a chemical reaction associated with oral contraceptive pills, or even lactation. Various factors, including hormonal imbalance, autoimmunity, unknown microbiological agents, smoking and α 1-antitrypsin deficiency have been suggested to play a role in disease aetiology. In this review, causing factors in the aetiology of idiopathic granulomatous mastitis are reviewed in detail. | Fatih Altintoprak Taner Kivilcim Orhan Veli Ozkan | 2014 | World Journal of Clinical Cases2014，2，12： | 52 |
| 13 | Targeting inflammation in diabetes: Newer therapeutic options显示文摘Inflammation has been recognised to both decrease beta cell insulin secretion and increase insulin resis-tance. Circulating cytokines can affect beta cell function directly leading to secretory dysfunction and increased apoptosis. These cytokines can also indirectly affect beta cell function by increasing adipocyte inflamma-tion.The resulting glucotoxicity and lipotoxicity further enhance the inflammatory process resulting in a vicious cycle. Weight reduction and drugs such as metformin have been shown to decrease the levels of C-Reactive Protein by 31% and 13%, respectively. Pioglitazone, insulin and statins have anti-inflammatory effects. In-terleukin 1 and tumor necrosis factor-α antagonists are in trials and NSAIDs such as salsalate have shown an improvement in insulin sensitivity. Inhibition of 12-lipo-oxygenase, histone de-acetylases, and activation of sirtuin-1 are upcoming molecular targets to reduce in-flammation. These therapies have also been shown to decrease the conversion of pre-diabetes state to diabe-tes. Drugs like glicazide, troglitazone, N-acetylcysteine and selective COX-2 inhibitors have shown benefit in diabetic neuropathy by decreasing inflammatory mark-ers. Retinopathy drugs are used to target vascular en-dothelial growth factor, angiopoietin-2, various protein-ases and chemokines. Drugs targeting the proteinases and various chemokines are pentoxifylline, inhibitors of nuclear factor-kappa B and mammalian target of rapa-mycin and are in clinical trials for diabetic nephropathy. Commonly used drugs such as insulin, metformin, per-oxisome proliferator-activated receptors, glucagon like peptide-1 agonists and dipeptidyl peptidase-4 inhibitors also decrease inflammation. Anti-inflammatory thera-pies represent a potential approach for the therapy of diabetes and its complications. | Neeraj Kumar Agrawal Saket Kant | 2014 | World Journal of Diabetes2014，5，5： | 41 |
| 14 | Th1/Th2 cytokines and their genotypes as predictors of hepatitis B virus related hepatocellular carcinoma显示文摘Hepatocellular carcinoma(HCC), the predominant type of primary liver cancer, is one of the most serious lifethreatening malignancies, worldwide. In majority of the cases, HCC develops after prolonged and persistent chronic liver disease. hepatitis B virus(HBV) or HCV infection is prominent etiological factors, attributing to this condition. It has been well documented that HBV, being the inducer of chronic inflammation, is the main causative agent in causing HCC, particularly in Asian countries. The HBV infection leads to a wide range of clinical symptoms from carrier state to malignancy. Cytokines being immune-modulatory molecules, are the key mediators in the defense mechanism against viral infection. In this regard, this review will detail the substantial role of key Th1: interleukin 1(IL-1), IL-2, IL-12, tumor necrosis factor-α, interferon-γ; Th2: IL-4, IL-10 and non Th1/Th2: IL-6, transforming growth factor-β1 cytokines genotypes in analyzing the variability in the clinical manifestations in an HBV-afflicted individual, which might finally, culminates into HCC. Since cytokine production is regulated genetically, the cytokine promoter region single-nucleotide polymorphisms induced changes, greatly affects the cytokine production, thus resulting into differential outcome of immune balance. | Roli Saxena Jyotdeep Kaur | 2015 | World Journal of Hepatology2015，7，11： | 50 |
| 15 | Effect of mild moxibustion on intestinal microbiota and NLRP6 inflammasome signaling in rats with post-inflammatory irritable bowel syndrome显示文摘BACKGROUND About one-third of refractory irritable bowel syndrome(IBS)cases are caused by gastrointestinal(GI)infection/inflammation,known as post-infectious/postinflammatory IBS(PI-IBS).Although it is known that intestinal microbiota and host NOD-like receptor family pyrin domain containing 6(NLRP6)inflammsome signaling are closely related to PI-IBS and moxibustion has a therapeutic effect on PI-IBS,whether moxibustion regulates the intestinal flora and host NLRP6 events in PI-IBS remains unclear.AIM To examine the regulatory effect of moxibustion on intestinal microbiota and host NLRP6 inflammatory signaling in PI-IBS.METHODS Sprague-Dawley rats were divided into a normal control group,a model control group,a mild moxibustion group,and a sham mild moxibustion group.PI-IBS rats in the mild moxibustion group were treated with moxibusiton at bilateral Tianshu(ST 25)and Zusanli(ST36)for 7 consecutive days for 10 min each time.The sham group rats were given the same treatment as the mild moxibustion group except the moxa stick was not ignited.Abdominal withdrawal reflex(AWR)score was measured to assess the visceral sensitivity,and colon histopathology and ultrastructure,colonic myeloperoxidase(MPO)activity,and serum C-reactive protein(CRP)level were measured to evaluate low-grade colonic inflammation in rats.The relative abundance of selected intestinal bacteria in rat feces was detected by 16S rDNA PCR and the NLRP6 inflammsome signaling in the colon was detected by immunofluorescence,qRTPCR,and Western blot.RESULTS The AWR score was significantly decreased and the low-grade intestinal inflammation reflected by serum CRP and colonic MPO levels was inhibited in the mild moxibustion group compared with the sham group.Mild moxibustion remarkably increased the relative DNA abundances of Lactobacillus,Bifidobacterium,and Faecalibacterium prausnitzii but decreased that of Escherichia coli in the gut of PI-IBS rats.Additionally,mild moxibustion induced mRNA and protein expression of intestine lectin 1 but inhibited the expression of IL-1β,IL-18,and resistance-like moleculeβby promoting the NLRP6 and reducing the mRNA and protein expression of apoptosis-associated speck-like protein containing CARD(ASC)and cysteinyl-aspartate-specific proteinase 1(Caspase-1).The relative DNA abundances of Lactobacillus,Bifidobacteria,Faecalibacterium prausnitzii,and Escherichia coli in each group were correlated with the mRNA and protein expression of NLRP6,ASC,and Caspase-1 in the colon.CONCLUSION These findings indicated that mild moxibustion can relieve low-grade GI inflammation and alleviate visceral hypersensitivity in PI-IBS by regulating intestinal microbes and controlling NLRP6 inflammasome signaling. | Chun-Hui Bao Chun-Ye Wang Guo-Na Li Yi-Lu Yan Di Wang Xiao-Ming Jin Lu-Yi Wu Hui-Rong Liu Xiao-Mei Wang Zheng Shi Huan-Gan Wu | 2019 | World Journal of Gastroenterology2019，25，32： | 45 |
| 16 | Mechanism underlying treatment of ischemic stroke using acupuncture:transmission and regulation显示文摘The inflammatory response after cerebral ischemia/reperfusion is an important cause of neurological damage and repair.After cerebral ischemia/reperfusion,microglia are activated,and a large number of circulating inflammatory cells infiltrate the affected area.This leads to the secretion of inflammatory mediators and an inflammatory cascade that eventually causes secondary brain damage,including neuron necrosis,blood-brain barrier destruction,cerebral edema,and an oxidative stress response.Activation of inflammatory signaling pathways plays a key role in the pathological process of ischemic stroke.Increasing evidence suggests that acupuncture can reduce the inflammatory response after cerebral ischemia/reperfusion and promote repair of the injured nervous system.Acupuncture can not only inhibit the activation and infiltration of inflammatory cells,but can also regulate the expression of inflammation-related cytokines,balance the effects of pro-inflammatory and anti-inflammatory factors,and interfere with inflammatory signaling pathways.Therefore,it is important to study the transmission and regulatory mechanism of inflammatory signaling pathways after acupuncture treatment for cerebral ischemia/reperfusion injury to provide a theoretical basis for clinical treatment of this type of injury using acupuncture.Our review summarizes the overall conditions of inflammatory cells,mediators,and pathways after cerebral ischemia/reperfusion,and discusses the possible synergistic intervention of acupuncture in the inflammatory signaling pathway network to provide a foundation to explore the multiple molecular mechanisms by which acupuncture promotes nerve function restoration. | Bing-Qian Cao Feng Tan Jie Zhan Peng-Hui Lai | 2021 | Neural Regeneration Research2021，16，5： | 43 |
| 17 | An update on the regulatory mechanisms of NLRP3 inflammasome activation显示文摘The NOD-,LRR-,and pyrin domain-containing protein 3(NLRP3)inflammasome is a multiprotein complex involved in the release of mature interleukin-1βand triggering of pyroptosis,which is of paramount importance in a variety of physiological and pathological conditions.Over the past decade,considerable advances have been made in elucidating the molecular mechanisms underlying the priming/licensing(Signal 1)and assembly(Signal 2)involved in NLRP3 inflammasome activation.Recently,a number of studies have indicated that the priming/licensing step is regulated by complicated mechanisms at both the transcriptional and posttranslational levels.In this review,we discuss the current understanding of the mechanistic details of NLRP3 inflammasome activation with a particular emphasis on protein-protein interactions,posttranslational modifications,and spatiotemporal regulation of the NLRP3 inflammasome machinery.We also present a detailed summary of multiple positive and/or negative regulatory pathways providing upstream signals that culminate in NLRP3 inflammasome complex assembly.A better understanding of the molecular mechanisms underlying NLRP3 inflammasome activation will provide opportunities for the development of methods for the prevention and treatment of NLRP3 inflammasome-related diseases. | Seungwha Paik Jin Kyung Kim Prashanta Silwal Chihiro Sasakawa Eun-Kyeong Jo | 2021 | Cellular & Molecular Immunology2021，18，5： | 43 |
| 18 | Hepatic inflammation and progressive liver fibrosis in chronic liver disease显示文摘Chronic liver inflammation drives hepatic fibrosis,and current immunosuppressive,anti-inflammatory,and anti-viral therapies can weaken this driver.Hepatic fibrosis is reversed,stabilized,or prevented in 57%-79%of patients by conventional treatment regimens,mainly by their anti-inflammatory actions.Responses,however,are commonly incomplete and inconsistently achieved.The fibrotic mechanisms associated with liver inflammation have been clarified,and anti-fibrotic agents promise to improve outcomes as adjunctive therapies.Hepatitis C virus and immune-mediated responses can activate hepatic stellate cells by increasing oxidative stress within hepatocytes.Angiotensin can be synthesized by activated hepatic stellate cells and promote the production of reactive oxygen species.Anti-oxidants(Nacetylcysteine,S-adenosyl-L-methionine,and vitamin E)and angiotensin inhibitors(losartin)have had antifibrotic actions in preliminary human studies,and they may emerge as supplemental therapies.Anti-fibrotic agents presage a new era of supplemental treatment for chronic liver disease. | Albert J Czaja | 2014 | World Journal of Gastroenterology2014，20，10： | 46 |
| 19 | Type 2 diabetes mellitus:From a metabolic disorder to an inflammatory condition显示文摘Diabetes mellitus is increasing at an alarming rate and has become a global challenge.Insulin resistance intarget tissues and a relative deficiency of insulin secretion from pancreatic β-cells are the major features of type 2 diabetes(T2D).Chronic low-grade inflammation in T2 D has given an impetus to the field of immuno-metabolism linking inflammation to insulin resistance and β-cell dysfunction.Many factors advocate a causal link between metabolic stress and inflammation.Numerous cellular factors trigger inflammatory signalling cascades,and as a result T2 D is at the moment considered an inflammatory disorder triggered by disordered metabolism.Cellular mechanisms like activation of Tolllike receptors,Endoplasmic Reticulum stress,and inflammasome activation are related to the nutrient excess linking pathogenesis and progression of T2 D with inflammation.This paper aims to systematically review the metabolic profile and role of various inflammatory pathways in T2 D by capturing relevant evidence from various sources.The perspectives include suggestions for the development of therapies involving the shift from metabolic stress to homeostasis that would favour insulin sensitivity and survival of pancreatic β-cells in T2 D. | Iqra Hameed Shariq R Masoodi Shahnaz A Mir Mudasar Nabi Khalid Ghazanfar Bashir A Ganai | 2015 | World Journal of Diabetes2015，6，4： | 36 |
| 20 | 2015年Banff会议肾移植报告解读显示文摘第十三届Banff会议在加拿大温哥华举行,来自28个国家的共计451名病理学家、免疫学家、临床及外科专家参加本次会议。会议首先回顾分析了2013年修改的抗体介导性排斥(antibodymediated rejection,ABMR)诊断标准对临床的影响,随后, | 王政禄 | 2017 | 实用器官移植电子杂志2017，5，2： | 38 |
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