Angiotensin-converting enzyme 2 alleviates liver fibrosis through the renin-angiotensin system

The present letter to the editor is related to the study titled‘Angiotensin-converting enzyme 2 improves liver fibrosis in mice by regulating autophagy of hepatic stellate cells’.Angiotensin-converting enzyme 2 can alleviate liver fibrosis by regulating autophagy of hepatic stellate cells and affecting the renin-angiotensin system.

Punicalagin prevents obesity-related cardiac dysfunction through promoting DNA demethylation in mice

The aim of this study was to investigate whether punicalagin(PU)could prevent obesity-related cardiac dysfunction by promoting DNA demethy lation,and to explore its possible mechanism.C57BL/6J mice were fed with standard diet,high-fat diet(HFD),HFD supplemented with resveratrol,low-dose PU(LPU)and high-dose PU(HPU)for 8 weeks.Compared with HFD group,body weight was significantly lower in PU treatment groups,number of cardionwocytes and the protein level of myosin heavy chain 7B were significantly higher in PU treatment groups.Levels of 5-hydroxymethylcytosine and 5-formylcytosine were significantly lower in HFD group than in other groups.Compared with the HFD group,the protein level of ten-eleven translocation enzyme(TET)2 was significantly higher in PU treatment groups,p-AMP-activated protein kinase(AMPK)was significantly higher in LPU group.Levels of total antioxidant capacity and the protein levels of complexesⅡ/Ⅲ/Ⅴ,oxoglutarate dehydrogenase,succinate dehydrogenase B and fumarate hdrolase were significantly lower in HFD group than PU treatment group.The ratio of(succinic acid+fumaric acid)/a-ketoglutarate was significantly higher in HFD group than other groups.In conclusion,PU up-regulated TETs enzyme activities and TET2 protein stability through alleviating mitochondrial dysfunction and activating AMPK,so as to promote DNA demethylation,thus preventing obesity-related cardiac dysfunction.

Exosomes derived from microglia overexpressing miR-124-3p alleviate neuronal endoplasmic reticulum stress damage after repetitive mild traumatic brain injury

We previously reported that miR-124-3p is markedly upregulated in microglia-derived exosomes following repetitive mild traumatic brain injury.However,its impact on neuronal endoplasmic reticulum stress following repetitive mild traumatic brain injury remains unclear.In this study,we first used an HT22 scratch injury model to mimic traumatic brain injury,then co-cultured the HT22 cells with BV2 microglia expressing high levels of miR-124-3p.We found that exosomes containing high levels of miR-124-3p attenuated apoptosis and endoplasmic reticulum stress.Furthermore,luciferase reporter assay analysis confirmed that miR-124-3p bound specifically to the endoplasmic reticulum stress-related protein IRE1α,while an IRE1αfunctional salvage experiment confirmed that miR-124-3p targeted IRE1αand reduced its expression,thereby inhibiting endoplasmic reticulum stress in injured neurons.Finally,we delivered microglia-derived exosomes containing miR-124-3p intranasally to a mouse model of repetitive mild traumatic brain injury and found that endoplasmic reticulum stress and apoptosis levels in hippocampal neurons were significantly reduced.These findings suggest that,after repetitive mild traumatic brain injury,miR-124-3 can be transferred from microglia-derived exosomes to injured neurons,where it exerts a neuroprotective effect by inhibiting endoplasmic reticulum stress.Therefore,microglia-derived exosomes containing miR-124-3p may represent a novel therapeutic strategy for repetitive mild traumatic brain injury.

Effects of tachykinin neuropeptide NKB and A<i>β</i>(25-35) on antioxidant enzymes status in 17<i>β</i>estradiol treated aging female rats

Aging is the leading risk factor for neurodegenerative diseases and oxidative stress involved in the pathophysiology of these diseases. These changes increase during menopausal condition in females when the level of estradiol is decreased. The aim of the present study was to determine the effect of tachykinin neuropeptide, Neurokinin B (NKB) and Amyloid beta fragment Aβ (25 -?35) on 17β estradiol (E2) treated aging female rat synaptosomes of different age groups. Aging brain functions were assayed by measuring the activities of antioxidant enzymes—superoxide dismutase (SOD) and monoamine oxidase (MAO) with neuropeptides. An in-vitro incubation of Aβ (25 -?35) in E2 treated brain synaptosomes showed toxic effects on all the parameters. However, NKB and NKB combined with Aβ (25 35) showed stimulating effects in E2 treated rat brain synaptosomes. In the present study, an increase in activity of SOD and decrease in the level of MAO, in the presence of NKB and combined NKB and Aβ in E2 treated brain synaptosomes of aging rats. This study elucidates that treatment of NKB and Aβ with E2 incombination exerts more protective influence than their individual application, against excitotoxicity in age related changes.

Correlation of serum Aβ1-42 content with inflammatory factors and receptors as well as antioxidant enzymes in patients with Parkinson's Disease

Objective: To investigate the correlation of serum β-amyloid 1-42 (Aβ1-42) content with inflammatory factors and receptors as well as antioxidant enzymes in patients with Parkinson's Disease. Methods: A total of 48 patients with Parkinson's disease who were treated in this hospital between December 2014 and October 2017 were selected as Parkinson's disease group, and 50 healthy volunteers who received physical examination in this hospital during the same period were selected as normal control group. The differences in serum contents of Aβ1-42, inflammatory factors and receptors as well as antioxidant enzymes were compared between the two groups, and Pearson test was used to assess the correlation between serum Aβ1-42 content and illness in patients with Parkinson's disease. Results: Serum Aβ1-42 content of Parkinson's disease group was lower than that of normal control group;serum inflammatory factors and receptors IL-2, sIL-2R, IL-6 and sIL-6R contents were higher than those of normal control group;serum antioxidant enzymes SOD, GSH-Px, CAT and TPX contents were lower than those of control group. Pearson test showed that serum Aβ1-42 content of patients with Parkinson's disease was directly correlated with the contents of inflammatory factors and receptors as well as antioxidant enzymes. Conclusions: Serum Aβ1-42 content decreases in patient with Parkinson's disease, and the specific content is directly correlated with the condition of Parkinson's disease, and can be used as an important auxiliary indicator for diagnosis and judgment of Parkinson's disease.

In vitro cleavage of hepatitis B virus C mRNA by 10-23 DNA enzyme

BACKGROUND: 10-23 DNA enzyme is one kind of de-oxyribozymes for RNA cleavage. The inhibition effects of 10-23 DNA enzyme on the expression of the HBV C gene in HepG2. 2. 15 cells were demonstrated previously. The aim of this study was to further explore the cleavage activities of 10-23 DNA enzyme targeting at HBV C gene mRNA in vitro. METHODS: 10-23 DNA enzyme named Drz-HBV-C-9 specific to HBV C gene ORF A1816UG was designed and synthesized. HBV C gene mRNA was obtained by the in vitro transcription method. Cleavage activities of Drz-HBV-C-9 were observed in vitro. Values of kinetic parameters including Km,Kcat and Kcat/Km were calculated accordingly. RESULTS: Under the certain cleavage conditions, Drz-HBV-C-9 could efficiently cleave target mRNA at specific sites in vitro. Cleavage products of 109nt plus 191nt were obtained. The kinetic parameters, Km,Kcat and Kcat/ Km for Drz-HBV-C-9, were 1.4 ×10-9 mol, 1.6 min-1 and 1.1 × 109 mol-1 · min-1, respectively. CONCLUSIONS: 10-23 DNA enzyme targeting at HBV C gene mRNA possesses specific cleavage activities in vitro. This would be a potent antiviral strategy with respect to HBV gene therapy.

A new angiotensin-converting enzyme inhibitor from Peperomia pellucida(L.) Kunth

Objective:To isolate,identify,and evaluate a new angiotensin-converting enzyme inhibitor from Peperomia pellucida(L.)Kunth herbs.Methods:A dried sample of Peperomia pellucida herb was successively macerated with n-hexane and ethyl acetate.The ethyl acetate extract solution was evaporated to obtain the crude extract.Vacuum liquid column chromatography and thin layer chromatography were performed to obtain two pure compounds.Then,both compounds were elucidated and identified using the spectroscopic method.Angiotensin-converting enzyme inhibitory activity studies of both compounds were determined using angiotensin-converting enzyme kit WST-1 with spectrophotometer microplate reader 96-well at 450 nm wavelength.Results:Two bioactive compounds were successfully isolated from Peperomia pellucida herb,including a new compound of 2,3,5-trimethoxy-9-(12,14,15-trimethoxybenzyl)-1 H-indene and pellucidin A.Both compounds demonstrated angiotensin-converting enzyme inhibitory activity,with IC50 values of 72 μM(27.95 μg/mL)and 1 1μM(4.4 μg/mL),respectively.Conclusions:In the present study,two active angiotensin-converting enzyme inhibitors were successfully isolated and purified from Peperomia pellucida which is used as an antihypertensive in traditional medicine,and support its use as an angiotensin-converting enzyme-inhibiting drug.

Electrochemical Enzyme Immunoassay of Tumor Marker CA15-3 with Capillary Electrophoresis

Tumor marker CA15-3 was determined by using capillary electrophoretic enzyme immunoassay with electrochemical detection (CE-EIA-ED). The method can be used to detect CA15-3 with a limit of 0.024 U/mL.

不同氮素水平对豫麦49-198籽粒灌浆及淀粉合成相关酶活性的调控效应

为了明确不同氮素水平下小麦干物质运转、籽粒灌浆及有关淀粉酶活性的变化规律,以豫麦49-198为材料,在河南科技大学试验农场,通过设置120 kg/hm2(N1)、180 kg/hm2(N2)、240 kg/hm2(N3)和300 kg/hm2(N4)4个氮素水平,研究了小麦茎鞘物质运转、籽粒灌浆和淀粉合成有关酶活性。结果表明,在一定范围内增施氮肥有利于提高茎鞘干物重以及抽穗后茎鞘物质输出量、输出率、转化率,各指标均以N3处理最高,N1处理最低。适量增施氮肥能提高籽粒生长潜势、最大灌浆速率和平均灌浆速率,缩短籽粒生长活跃期,使品种达最大灌浆速率的时间提前,其中N3处理最佳,其最大灌浆速率和平均灌浆速率分别为0.557×10-2和0.373×10-2g/(grains.d),N4处理最差,其最大灌浆速率和平均灌浆速率分别为0.406×10-2和0.272×10-2g/(grains.d)。适量增施氮肥能增强籽粒灌浆过程中可溶性淀粉合成酶(SSS)、Q酶和ADPG焦磷酸化酶3种酶活性,各处理中,酶活性均以N3处理最高,N4处理最低,N3和N4处理相比SSS、Q和ADPG焦磷酸化酶最大酶活性分别提高了22.0%、23.2%和9.5%。但过量施氮,降低了茎鞘干物重的积累、运输和转化能力以及籽粒灌浆速率和3种淀粉合成有关酶活性。抽穗期茎鞘干物重、抽穗后茎鞘干物质输出量和输出率均与籽粒产量呈显著正相关。试验表明,在适宜氮肥水平下小麦具有较高的茎鞘物质输出率和转化率、籽粒灌浆速率及淀粉合成有关酶活性,是产量较高的生理基础。

Calcium-dependent activation of CPK12 facilitates its cytoplasm-to-nucleus translocation to potentiate plant hypoxia sensing by phosphorylating ERF-Ⅶ transcription factors

Calcium-dependent protein kinases(CDPKs/CPKs)are key regulators of plant stress signaling that translate calcium signals into cellular responses by phosphorylating diverse substrate proteins.However,the molecular mechanism by which plant cells relay calcium signals in response to hypoxia remains elusive.Here,we show that one member of the CDPK family in Arabidopsis thaliana,CPK12,is rapidly activated during hypoxia through calcium-dependent phosphorylation of its Ser-186 residue.Phosphorylated CPK12 shuttles from the cytoplasm to the nucleus,where it interacts with and phosphorylates the group Ⅶ ethylene-responsive transcription factors(ERF-Ⅶ)that are core regulators of plant hypoxia sensing,to enhance their stabilities.Consistently,CPK12 knockdown lines show attenuated tolerance of hypoxia,whereas transgenic plants overexpressing CPK12 display improved hypoxia tolerance.Nonethelss,loss of function of five ERF-Ⅶ proteins in an erf-vii pentuple mutant could partially suppress the enhanced hypoxia-tolerance phenotype of CPK12-overexpressing lines.Moreover,we also discovered that phosphatidic acid and 14-3-3κ protein serve as positive and negative modulators of the CPK12 cytoplasm-to-nucleus translocation,respectively.Taken together,these findings uncover a CPK12-ERF-Ⅶ regulatory module that is key to transducing calcium signals from the cytoplasm into the nucleus to potentiate hypoxia sensing in plants.

母体表达基因3通过miR-125a-5p/TET2途径抑制HepG2细胞载脂蛋白(a)的表达

目的研究发现母体表达基因3（MEG3）对HepG2细胞载脂蛋白（a）[Apo（a）]表达的调控作用及其机制。方法用荧光素酶报告系统分析MEG3与miR-125a-5p的靶向性结合。采用实时定量PCR（qRT-PCR）检测高表达Apo（a）的HepG2细胞和低表达Apo（a）的SMMC7721细胞中MEG3的表达情况;向HepG2细胞转染MEG3,Western blot和qRT-PCR检测Apo（a）、TET2表达情况;采用小干扰RNA技术沉默TET2的表达。结果 （1）MEG3与hsa-miR-125a-5p能互补性结合,荧光素酶报告基因系统分析结果证实了MEG3与hsa-miR-125a-5p结合的存在。（2）miR芯片结果表明,在HepG2细胞中,hsa-miR-125a-5p表达水平升高,是对照组的近1.5倍,MEG3在HepG2细胞和SMMC7721细胞中均有表达,但前者MEG3的表达水平显著低于后者。（3）MEG3抑制Apo（a）表达。（4）MEG3下调miR-125a-5p的表达,上调TET2的表达; miR-125a-5p的mimics可逆转MEG3对Apo（a）的下调作用及TET2的表达,但可被miR-125a-5p的抑制剂逆转; TET2沉默可逆转MEG3对Apo（a）的下调作用。结论 MEG3通过miR-125a-5p/TET2途径下调HepG2细胞Apo（a）的表达。

Renin-angiotensin system in the pathogenesis of liver fibrosis

Hepatic fibrosis is considered a common response to many chronic hepatic injuries. It is a multifunctional process that involves several cell types, cytokines, chemokines and growth factors leading to a disruption of homeostatic mechanisms that maintain the liver ecosystem. In spite of many studies regarding the development of fibrosis, the understanding of the pathogenesis remains obscure. The hepatic tissue remodeling process is highly complex, resulting from the balance between collagen degradation and synthesis. Among the many mediators that take part in this process, the components of the Renin angiotensin system （RAS） have progressively assumed an important role. Angiotensin （Ang） II acts as a profibrotic mediator and Ang-（1-7）, the newly recognized RAS component, appears to exert a counter-regulatory role in liver tissue. We briefly review the liver fibrosis process and current aspects of the RAS. This review also aims to discuss some experimental evidence regarding the participation of RAS mediators in the pathogenesis of liver fibrosis, focusing on the putative role of the ACE2-Ang-（1-7）- Mas receptor axis.

Relationship between angiotensin-(1-7) and angiotensin Ⅱ correlates with hemodynamic changes in human liver cirrhosis

AIM： To measure circulating angiotensins at different stages of human cirrhosis and to further evaluate a possible relationship between renin angiotensin system （RAS） components and hemodynamic changes. METHODS： Patients were allocated into 4 groups： mild-to-moderate liver disease （MLD）, advanced liver disease （ALD）, patients undergoing liver transplantation, and healthy controls. Blood was collected to determine plasma renin activity （PRA）, angiotensin （Ang） Ⅰ, Ang Ⅱ, and Ang-（1-7） levels using radioimmunoassays. During liver transplantation, hemodynamic parameters were determined and blood was simultaneously obtained from the portal vein and radial artery in order to measure RAS components. RESULTS： PRA and angiotensins were elevated in ALD when compared to MLD and controls （P 〈 0.05）. In contrast, Ang Ⅱ was significantly reduced in MLD. Ang-（1-7）/Ang Ⅱ ratios were increased in MLD when compared to controls and ALD. During transplantation, Ang Ⅱ levels were lower and Ang-（1-7）/Ang Ⅱ ratios were higher in the splanchnic circulation than in the peripheral circulation （0.52 ± 0.08 vs 0.38 ±0.04, P 〈 0.02）, whereas the peripheral circulating Ang Ⅱ/Ang Ⅰ ratio was elevated in comparison to splanchnic levels （0.18 ±0.02 vs 0.13 ±0.02, P 〈 0.04）. Ang-（1-7）/ Ang Ⅱ ratios positively correlated with cardiac output （r = 0.66） and negatively correlated with systemic vascular resistance （r = -0.70）. CONCLUSION： Our findings suggest that the relationship between Ang-（1-7） and Ang Ⅱ may play a role in the hemodynamic changes of human cirrhosis.

Effect of Cl￣ on Behavior of Fertilizer Nitrogen, Nnmberof Microorganisms and Enzyme Activities in Soils

Pot experiments were conducted to study the effect of Cl￣- on transformation of fertilizer N, number ofmicroorganisms and enzyme activities in soils. It is indicated that Cl￣- did not show significant influenceon total number of bacteria, actinomyces and fungi, but significantly reduced the number of nitrosobacteria,which led to decrease of NO content in the soil. Application of Cl￣- to soil could significantly enhance theactivities of phosphatase and urease in the coastal saline soil and orthic aquisols. In hilly red soil, however,the application of Cl￣- at the rate of 500-1000 mg Cl￣- kg￣(-1) soil significantly decreased the activity of thetwo enzymes mentioned above.

Serum levels of angiotensin converting enzyme as a biomarker of liver fibrosis

The renin angiotensin system(RAS) is classically conceived as a circulating hormonal system involved in blood pressure control and hydroelectrolyte balance. The discovery that RAS components are locally expressed in a wide range of organs and tissues,including the liver,pointed to a role for this system in the pathogenesis of several conditions including hepatic fibrosis and cirrhosis. It has been widely reported that the classical RAS axis composed by the angiotensin converting enzyme(ACE)-angiotensin(Ang) Ⅱ-Ang type 1(AT1) receptor mediates pro-inflammatory,pro-thrombotic,and pro-fibrotic processes. On the other hand,the alternative axis comprising ACE2-Ang-(1-7)-Mas receptor seems to play a protective role by frequently opposing Ang Ⅱ action. Chronic hepatitis B(CHB) is one of the leading causes of liver fibrosis,accounting for the death of nearly one million people worldwide. Liver fibrosis is a key factor to determine therapeutic interventions for patients with CHB. However,the establishment of non-invasive and accurate methods to detect reversible stages of liver fibrosis is still a challenge. In an elegant study published in the 36 th issue of the World Journal of Gastroenterology,Noguchi et al showed the predictive value of serum ACE levels in detecting not only advanced stages of liver fibrosis but also initial and intermediate fibrotic stages. The serum levels of ACE might represent an accurate,non-invasive,widely available,and easy method to evaluate fibrosis related to CHB. Moreover,therapies involving the inhibition of the classical RAS axis components might be promising in the control of CHB-related liver fibrosis.

Purification and characterization of cold-active endo-1,4-β-glucanase produced by Pseudoalteromonas sp. AN545 from Antarctica

A bacterium hydrolyzing carboxymethylcellulose, isolated from Antarctic sea ice, was identified as Pseudoalteromonas sp. based on 16S rDNA gene sequences and named as Pseudoalteromonas sp. AN545. The extracellular endo-1,4-β-glucanase AN-1 was purified successively by ammonium sulfate precipitation, DEAE-Sepharose ion exchange chromatography and Sephadex G-75 gel filtration chromatography. The molecular mass of AN-1 was estimated to be 47.5 kDa utilizing SDS-PAGE and gel chromatography analysis. AN-1 could hydrolyze caboxymethylcellulose, avicel and β-glucan, but not cellobiose, xylan and p-Nitrophenyl-β-D-glucopyranoside. The optimal temperature and pH for the β-glucanase activity of AN-1 were determined to be at 30℃ and pH 6.0, respectively. AN-1 was stable at acidic solutions of pH 5.0-6.5 and temperatures below 30℃ for 1 h. Moreover, the specific activity was enhanced by Ca2＋ and Mg2., and inhibited by Cu2＋. The kinetic parameters Michaelis constant （Km） and maximum velocity （Vmax） of AN-1 were 3.96 mg/mL and 6.06×10-2 mg/（min.mL）, respectively.

Integrating network pharmacology and pharmacological evaluation for deciphering the mechanism of(-)-epigallocatechin-3-gallate alleviating ethanol-induced endothelial cells injury

Objective To investigate the potential therapeutic targets and pharmacological mechanism of(-)-epigallocatechin-3-gallate(EGCG)based on network pharmacology and experimental verification.METHODS The druggability of EGCG was measured by the traditional Chinese medicine systems pharmacology(TCMSP)server,and potential targets of EGCG were identified by Pharm Mapper and Drug Repositioning and Adverse drug Reaction via Chemical-Protein Interactome(DRAR-CPI).The potential targets were imported into GeneMANIA database to obtain the protein-protein direct interaction network,and target physical interaction,co-expression,prediction,genetic interaction,and shared protein domains.The biological process,molecular functions,cellular components and KEGG signaling pathways of potential targets were analyzed using DAVID database.For further study,ethanol was used to establish a model of endothelial injury in vitro.The cell viability was assayed by MTT method,the cellular apoptosis was stained by Annexin V/PI,and the expression levels of Bcl-2,Bax and cleved-caspase-3 were tested by Western blotting.Then,JC-1 and nuclear translocation of NF-κB experiments were used to study the mitochondrial membrane potential and nuclear translocation.RESULTS The oral availability of EGCG was 55.09%(≥30%)and drug-like index was 0.77(≥0.18),which were considered pharmacokinetically active.17 potential targetable proteins of EGCG were predicted by Pharm Mapper and DRAR-CPI.Further research showed that 68.13%displayed similar co-expression characteristics,26.11%physical interactions,and 2.74%shared the same protein domain.The depth network analysis results showed that the biofunctions of EGCG were mainly by regulating glutathione derivative biosynthetic process,glutathione metabolic process,nitrogen compound metabolic process etc..via drug binding,catalytic activity,glutathione transferase activity,anion binding etc..in sarcoplasmic reticulum,spindle pole,microtubule cytoskeleton and cytoplasm.KEGG enrichment analysis showed that Glutathione metabolism,IL^(-1)7 signaling pathway,EGFR tyrosine kinase inhibitor resistance,PI3K-Akt signaling pathway and other pathways were involves in the biofunction of EGCG.The above analyses indicated that EGCG exerts its biofunction through antioxidant and anti-inflammatory mechanisms.The experimental results showed that ethanol 20.0 mmol·L^(-1) decreased cell viability,Bcl-2 expression,and increased cell apoptosis,the intracellular ROS,as well as the expression of Bax and cleaved-caspase-3 of human endothelial cells.However,treatment of the cells with EGCG can significantly alleviate ethanol induced endothelial cells injury.Further study showed that EGCG significantly alleviates ethanol induced mitochondrial depolarization and nuclear translocation of NF-κB.CONCLUSIONS EGCG exerts pharmacological efficacies on ethanol induced endothelial cell injury through multi-target,multi-function and multi-pathway mode.Protective effect of EGCG on ethanol induced cell injury was mainly through alteration of mitochondrial function and NF-κB translocation.Therefore,EGCG have great potential in protecting against endothelial dysfunction of the persons who are chronically abuse of ethanol.This study also provides a new understanding of EGCG in clinical application on cardiovascular and cerebrovascular diseases.

Crystal Structures of Urokinase-type Plasminogen Activator in Complex with 4-(Aminomethyl) Benzoic Acid and 4-(Aminomethyl-phenyl)-methanol

Urokinase-type plasminogen activator （uPA） is a trypsin-like serine protease and plays a key role in several biological processes, including tissue remodeling, cell migration, and matrix degradation. The inhibitors of uPA have been shown to prevent the spread of metastasis and tumor growth, and accordingly uPA is widely recognized as a target for the treatment of cancer. In this work, we report the crystal structures of the complexes of uPA with its inhibitors： 4- （aminomethyl）-benzoic acid （AMBA） and 4-（aminomethyl-phenyl）-methanol （AMPM）, both at a resolution of 2.35 А. The inhibitory constants of these two inhibitors were measured by a chromogenic competitive assay, and it was found that AMBA is a better inhibitor for uPA （Ki = 2.68 mM） than AMPM （Ki = 13.99 mM）. The structural study shows that the binding mode of inhibitor AMBA on uPA is similar to that of AMPM on uPA, both docked into the active site S1 pocket of uPA. Structural details of these complexes are provided to explain the difference of inhibitory constants.

Ocular renin-angiotensin system with special reference in the anterior part of the eye

The renin-angiotensin system(RAS) regulates blood pressure(BP) homeostasis, systemic fluid volume and electrolyte balance. The RAS cascade includes over twenty peptidases, close to twenty angiotensin peptides and at least six receptors. Out of these, angiotensin Ⅱ, angiotensin converting enzyme 1 and angiotensin Ⅱ type 1 receptor(AngⅡ-ACE1-AT1R) together with angiotensin(1-7), angiotensin converting enzyme 2 and Mas receptor(Ang(1-7)-ACE2-Mas R) are regarded as the main components of RAS. In addition to circulating RAS, local RA-system exists in various organs. Local RA-systems are regarded as tissue-specific regulatory system accounting for local effects and long term changes in different organs. Many of the central components such as the two main axes of RAS: AngⅡ-ACE1-AT1 R and Ang(1-7)-ACE2-Mas R, have been identified in the human eye. Furthermore, it has been shown that systemic antihypertensive RAS- inhibiting medications lower intraocular pressure(IOP). These findings suggest the crucial role of RAS not only in the regulation of BP but also in the regulation of IOP, and RAS potentially plays a role in the development of glaucoma and antiglaucomatous drugs.

Advances in angiotensin-(1-7) and atrial fibrillation

Atrial fibrillation (AF) is one of the most common arrhythmias in clinic. Atrial fibrillation and its complications are one of the important causes of death. Despite the development of new therapies, including catheter ablation, the treatment of atrial fibrillation remains an important and arduous task. Current studies on the mechanism of atrial fibrillation show that the occurrence and development of atrial fibrillation mainly involves the electrophysiological mechanism of the heart and the pathophysiological mechanism of the heart. Atrial remodeling plays an important role in the process of atrial fibrillation. Atrial remodeling includes electrical remodeling of atrial structure. The early stage of atrial remodeling is characterized by electrophysiological and ion channel changes, while the late stage is characterized by amyloidosis and fibrosis of extracellular matrix and atrial muscle. Angiotensin-converting enzyme 2 and angiotensin-(1-7) are important components of renin-angiotensin-aldosterone system. Recent studies have shown that angiotensin - (1-7) plays an important protective role in the occurrence and development of atrial fibrillation. In this paper, the relationship between angiotensin - (1-7) and atrial remodeling during atrial fibrillation and its research progress are reviewed.