Clinical Science (London, England : 1979)最新文献_第2页

Modulating hepatic macrophages with annexin A1 in non-alcoholic steatohepatitis. 用膜联蛋白A1调节非酒精性脂肪性肝炎中的肝巨噬细胞。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-08-12 DOI: 10.1042/CS20220258

Federico F De Ponti, Charlotte L Scott

{"title":"Modulating hepatic macrophages with annexin A1 in non-alcoholic steatohepatitis.","authors":"Federico F De Ponti, Charlotte L Scott","doi":"10.1042/CS20220258","DOIUrl":"https://doi.org/10.1042/CS20220258","url":null,"abstract":"Non-alcoholic steatohepatitis (NASH) and associated end-stage liver disease is a growing cause of concern throughout the Western world. It constitutes a significant clinical burden for which therapeutic approaches are very limited. Over the last years, considerable attention has therefore been paid to identifying potential therapeutic strategies to reduce this burden. Annexin A1 (AnxA1), a calcium-phospholipid binding protein, has been proposed to be a negative regulator of inflammation in the context of NASH. In a recent publication, Gadipudi, Ramavath, Provera et al. investigated the therapeutic potential of Annexin A1 treatment in preventing the progression of NASH. They demonstrate that treatment of mice with NASH with recombinant human AnxA1 can reduce inflammation and fibrosis without affecting steatosis or metabolic syndrome. This was proposed to be achieved through the modulation of the macrophage populations present in the liver. Here, we discuss the main findings of this work and raise some outstanding questions regarding the possible mechanisms involved and the functions of distinct macrophage populations in NASH.","PeriodicalId":519494,"journal":{"name":"Clinical Science (London, England : 1979)","volume":" ","pages":"1111-1115"},"PeriodicalIF":6.0,"publicationDate":"2022-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/0c/a4/cs-136-cs20220258.PMC9366860.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40672920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

The multifaceted actions of the lncRNA H19 in cardiovascular biology and diseases. lncRNA H19在心血管生物学和疾病中的多方面作用。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-08-12 DOI: 10.1042/CS20210994

Denise Busscher, Reinier A Boon, Rio P Juni

{"title":"The multifaceted actions of the lncRNA H19 in cardiovascular biology and diseases.","authors":"Denise Busscher, Reinier A Boon, Rio P Juni","doi":"10.1042/CS20210994","DOIUrl":"https://doi.org/10.1042/CS20210994","url":null,"abstract":"Cardiovascular diseases are the leading cause of death and debility worldwide. Various molecular mechanisms have been studied to better understand the development and progression of cardiovascular pathologies with hope to eradicate these diseases. With the advancement of the sequencing technology, it is revealed that the majority of our genome is non-coding. A growing body of literature demonstrates the critical role of long non-coding RNAs (lncRNAs) as epigenetic regulators of gene expression. LncRNAs can regulate cellular biological processes through various distinct molecular mechanisms. The abundance of lncRNAs in the cardiovascular system indicates their significance in cardiovascular physiology and pathology. LncRNA H19, in particular, is a highly evolutionarily conserved lncRNA that is enriched in cardiac and vascular tissue, underlining its importance in maintaining homeostasis of the cardiovascular system. In this review, we discuss the versatile function of H19 in various types of cardiovascular diseases. We highlight the current literature on H19 in the cardiovascular system and demonstrate how dysregulation of H19 induces the development of cardiovascular pathophysiology.","PeriodicalId":519494,"journal":{"name":"Clinical Science (London, England : 1979)","volume":" ","pages":"1157-1178"},"PeriodicalIF":6.0,"publicationDate":"2022-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9366862/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40599986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

Early biochemical observations point to nutritional strategies to manage non-alcoholic fatty liver disease. 早期的生化观察指出，营养策略可以治疗非酒精性脂肪肝。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-07-15 DOI: 10.1042/CS20220380

Philip C Calder

{"title":"Early biochemical observations point to nutritional strategies to manage non-alcoholic fatty liver disease.","authors":"Philip C Calder","doi":"10.1042/CS20220380","DOIUrl":"https://doi.org/10.1042/CS20220380","url":null,"abstract":"Non-alcoholic fatty liver disease (NAFLD) is the most prevalent liver disease globally. The first stage of NAFLD is steatosis, the accumulation of triacylglycerols within hepatocytes. Inflammation and oxidative stress both contribute to progression to more severe disease. In 2004 Clinical Science published two papers reporting on fatty acids and oxidative stress markers in the livers of patients with NAFLD; both these papers are highly cited. One paper reported an altered pattern of fatty acids within the livers of patients with NAFLD; there was a lower contribution of polyunsaturated fatty acids (PUFAs) including both n - 6 and n - 3 PUFAs and an altered balance between n - 6 and n - 3 PUFAs in favour of the former. Ratios of precursor PUFAs to their long chain more unsaturated derivatives were altered in NAFLD and were interpreted to indicate a reduced activity of the pathway of synthesis of long chain highly unsaturated PUFAs. The authors interpreted their findings to indicate that a low hepatic content of n - 3 PUFAs has a causal role in NAFLD. The second paper reported lower hepatic antioxidant defences and increased markers of oxidative stress in NAFLD, consistent with a role for oxidative stress in the disease. Many studies have now explored the effect of supplemental n - 3 PUFAs or antioxidants, including vitamin E, in patients with NAFLD with some benefits being reported. There remains much interest in n - 3 PUFAs and antioxidants as preventive and therapeutic strategies in NAFLD and therefore it seems likely that citation of the two papers from 2004 will be sustained.","PeriodicalId":519494,"journal":{"name":"Clinical Science (London, England : 1979)","volume":" ","pages":"1019-1023"},"PeriodicalIF":6.0,"publicationDate":"2022-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40462675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Casting a wide NET: an update on uncontrolled NETosis in response to COVID-19 infection. 广泛撒网:应对COVID-19感染的不受控制的NETosis最新情况。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-07-15 DOI: 10.1042/CS20220039

Erin B Taylor

引用次数: 2

L-Glutamine alleviates osteoarthritis by regulating lncRNA-NKILA expression through the TGF-β1/SMAD2/3 signalling pathway. l -谷氨酰胺通过TGF-β1/SMAD2/3信号通路调节lncRNA-NKILA表达，缓解骨关节炎。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-07-15 DOI: 10.1042/CS20220082

Xiao Ma, Dechao Cai, Yakun Zhu, Yao Zhao, Xianbo Shang, Chen Wang, Haotian Zhang, Ashuai Bian, Haoran Yu, Wendan Cheng

{"title":"L-Glutamine alleviates osteoarthritis by regulating lncRNA-NKILA expression through the TGF-β1/SMAD2/3 signalling pathway.","authors":"Xiao Ma, Dechao Cai, Yakun Zhu, Yao Zhao, Xianbo Shang, Chen Wang, Haotian Zhang, Ashuai Bian, Haoran Yu, Wendan Cheng","doi":"10.1042/CS20220082","DOIUrl":"https://doi.org/10.1042/CS20220082","url":null,"abstract":"Osteoarthritis (OA) is a heterogeneous condition characterized by cartilage degradation, subchondral sclerosis, and osteophyte formation, and accompanied by the generation of pro-inflammatory mediators and degradation of extracellular matrix. The current treatment for early OA is focused on the relief of symptoms, such as pain, but this treatment cannot delay the pathological process. L-Glutamine (L-Gln), which has anti-inflammatory and anti-apoptotic effects, is the most abundant amino acid in human blood. However, its role in OA has not been systematically studied. Therefore, the objective of this work was to explore the therapeutic effect and molecular mechanism of L-Gln on OA. In vitro, we found that L-Gln could up-regulate the expression of the long non-coding RNA NKILA, which is regulated by the transforming growth factor-β1/SMAD2/3 pathway, and inhibit the activity of nuclear factor-κB, thereby decreasing the expression of nitric oxide synthase, cyclooxygenase-2, and matrix metalloproteinase-13 (MMP-13). This led to a reduction in the generation of nitrous oxide, prostaglandin E-2, tumour necrosis factor-α, and degradation of the extracellular matrix (i.e. aggrecan and collagen II) in rat OA chondrocytes. Moreover, intragastric administration of L-Gln reduced the degradation of cartilage tissue and expression of MMP-13 in a rat OA model. L-Gln also relieved the clinical symptoms in some patients with early knee joint OA. These findings highlight that L-Gln is a potential therapeutic drug to delay the occurrence and development of OA.","PeriodicalId":519494,"journal":{"name":"Clinical Science (London, England : 1979)","volume":" ","pages":"1053-1069"},"PeriodicalIF":6.0,"publicationDate":"2022-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9264285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40177704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Correction: Novel insights in endocrine and metabolic pathways in sepsis and gaps for future research. 更正:对败血症中内分泌和代谢途径的新见解以及未来研究的空白。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-07-15 DOI: 10.1042/CS-2021-1003C_COR

引用次数: 0

Defining the molecular underpinnings controlling cardiomyocyte proliferation. 确定控制心肌细胞增殖的分子基础。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-06-30 DOI: 10.1042/CS20211180

Donya Mahiny-Shahmohammady, Ludger Hauck, Filio Billia

{"title":"Defining the molecular underpinnings controlling cardiomyocyte proliferation.","authors":"Donya Mahiny-Shahmohammady, Ludger Hauck, Filio Billia","doi":"10.1042/CS20211180","DOIUrl":"https://doi.org/10.1042/CS20211180","url":null,"abstract":"Shortly after birth, mammalian cardiomyocytes (CM) exit the cell cycle and cease to proliferate. The inability of adult CM to replicate renders the heart particularly vulnerable to injury. Restoration of CM proliferation would be an attractive clinical target for regenerative therapies that can preserve contractile function and thus prevent the development of heart failure. Our review focuses on recent progress in understanding the tight regulation of signaling pathways and their downstream molecular mechanisms that underly the inability of CM to proliferate in vivo. In this review, we describe the temporal expression of cell cycle activators e.g., cyclin/Cdk complexes and their inhibitors including p16, p21, p27 and members of the retinoblastoma gene family during gestation and postnatal life. The differential impact of members of the E2f transcription factor family and microRNAs on the regulation of positive and negative cell cycle factors is discussed. This review also highlights seminal studies that identified the coordination of signaling mechanisms that can potently activate CM cell cycle re-entry including the Wnt/Ctnnb1, Hippo, Pi3K-Akt and Nrg1-Erbb2/4 pathways. We also present an up-to-date account of landmark studies analyzing the effect of various genes such as Argin, Dystrophin, Fstl1, Meis1, Pitx2 and Pkm2 that are responsible for either inhibition or activation of CM cell division. All these reports describe bona fide therapeutically targets that could guide future clinical studies toward cardiac repair.","PeriodicalId":519494,"journal":{"name":"Clinical Science (London, England : 1979)","volume":" ","pages":"911-934"},"PeriodicalIF":6.0,"publicationDate":"2022-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40058500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

The non-steroidal mineralocorticoid receptor antagonist finerenone is a novel therapeutic option for patients with Type 2 diabetes and chronic kidney disease. 非甾体矿物皮质激素受体拮抗剂芬尼酮是2型糖尿病和慢性肾病患者的一种新的治疗选择。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-06-30 DOI: 10.1042/CS20220212

Jonatan Barrera-Chimal, Casimiro Gerarduzzi, Patrick Rossignol, Frédéric Jaisser

{"title":"The non-steroidal mineralocorticoid receptor antagonist finerenone is a novel therapeutic option for patients with Type 2 diabetes and chronic kidney disease.","authors":"Jonatan Barrera-Chimal, Casimiro Gerarduzzi, Patrick Rossignol, Frédéric Jaisser","doi":"10.1042/CS20220212","DOIUrl":"https://doi.org/10.1042/CS20220212","url":null,"abstract":"Despite strong preclinical data supporting the use of mineralocorticoid receptor antagonists (MRAs) to provide cardiorenal protection in rodent models of diabetes, the clinical evidence of their utility in treating chronic kidney disease (CKD) has been limited. Two major clinical trials (FIDELIO-DKD and FIGARO-DKD) including more than 13,000 patients with albuminuric CKD and Type 2 diabetes randomized to placebo or finerenone (MRA) have recently provided exciting results showing a significant risk reduction for kidney and cardiovascular outcomes. In this review, we will summarize the major findings of these trials, together with post-hoc and pooled analyses that have allowed evaluation of the efficacy and safety of finerenone across the spectrum of CKD, revealing significant protective effects of finerenone against kidney failure, new-onset atrial fibrillation or flutter, new-onset heart failure, cardiovascular death, and first and total heart-failure hospitalizations. Moreover, we will discuss the current evidence that supports the combined use of MRAs with sodium-glucose co-transporter-2 inhibitors, either by providing an additive cardiorenal benefit or by decreasing the risk of hyperkalemia. Although the mechanisms of protection by finerenone have only been partially explored in patients, rodent studies have shed light on its anti-inflammatory and anti-fibrotic effects in models of kidney disease, which is one of the main drivers for testing the efficacy of finerenone in non-diabetic CKD patients in the ongoing FIND-CKD trial.","PeriodicalId":519494,"journal":{"name":"Clinical Science (London, England : 1979)","volume":" ","pages":"1005-1017"},"PeriodicalIF":6.0,"publicationDate":"2022-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40408550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Molecular and cellular regulation of psoriatic inflammation. 银屑病炎症的分子和细胞调控。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-06-30 DOI: 10.1042/CS20210916

Tom Macleod, Charles Bridgewood, Isabel Hyde, Megan Heague, Philip Helliwell, Martin Stacey, Miriam Wittmann

引用次数: 2

Microbiota transplantation in portal hypertension: promises and pitfalls. 门静脉高压症的微生物群移植:希望与缺陷。

IF 6

Clinical Science (London, England : 1979) Pub Date : 2022-03-31 DOI: 10.1042/CS20220029

Emilie K Mitten, György Baffy

{"title":"Microbiota transplantation in portal hypertension: promises and pitfalls.","authors":"Emilie K Mitten, György Baffy","doi":"10.1042/CS20220029","DOIUrl":"https://doi.org/10.1042/CS20220029","url":null,"abstract":"In this commentary, we discuss new findings indicating that microbiota transplantation has favorable impact on portal hypertension (PH) in the experimental model of cirrhosis induced by bile duct ligation (BDL) (Huang et al.; Clin Sci (Lond) (2021) 135(24): 2709-2728, doi: 10.1042/CS20210602). Sinusoidal PH is an ominous outcome of advanced chronic liver disease, characterized by increased intrahepatic vascular resistance (IHVR), splanchnic hyperemia, and the development of portosystemic collaterals. In the work of Huang et al., microbiota transplantation not only alleviated splanchnic hyperdynamic circulation by improving vascular responsiveness and decreasing mesenteric angiogenesis, but also reduced blood flow in portosystemic collaterals. Surprisingly, however, microbiota transplantation had no effect on intrahepatic vasoconstriction in this experimental model. We discuss these observations in the context of recent literature showing that manipulation of the gut microbiota (either by transplantation or through the use of probiotics) may improve IHVR, which is one of the earliest abnormalities in the pathogenesis of sinusoidal PH. Further research is needed to explore the specific molecular and cellular targets associated with the correction of dysbiosis in liver disease.","PeriodicalId":519494,"journal":{"name":"Clinical Science (London, England : 1979)","volume":" ","pages":"425-429"},"PeriodicalIF":6.0,"publicationDate":"2022-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40327599","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2