Journal of the renin-angiotensin-aldosterone system : JRAAS最新文献

{"title":"View of the Renin-Angiotensin System in Acute Kidney Injury Induced by Renal Ischemia-Reperfusion Injury.","authors":"Farzaneh Karimi, Maryam Maleki, Mehdi Nematbakhsh","doi":"10.1155/2022/9800838","DOIUrl":"https://doi.org/10.1155/2022/9800838","url":null,"abstract":"Renal ischemia-reperfusion injury (RIRI) is a sequence of complicated events that is defined as a reduction of the blood supply followed by reperfusion. RIRI is the leading cause of acute kidney injury (AKI). Among the diverse mediators that take part in RIRI-induced AKI, the renin-angiotensin system (RAS) plays an important role via conventional (angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensin (Ang) II, and Ang II type 1 receptor (AT1R)) and nonconventional (ACE2, Ang 1-7, Ang 1-9, AT2 receptor (AT2R), and Mas receptor (MasR)) axes. RIRI alters the balance of both axes so that RAS can affect RIRI-induced AKI. In overall, the alteration of Ang II/AT1R and AKI by RIRI is important to consider. This review has looked for the effects and interactions of RAS activities during RIRI conditions.","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"9800838"},"PeriodicalIF":2.9,"publicationDate":"2022-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9617735/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40438664","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}

{"title":"Influence of <i>SERPINA1</i> Gene Polymorphisms on Anemia and Chronic Obstructive Pulmonary Disease.","authors":"Thangavelu Sangeetha,&nbsp;Tajuddin Nargis Begum,&nbsp;Balasubramanian Balamuralikrishnan,&nbsp;Meyyazhagan Arun,&nbsp;Kannan R R Rengasamy,&nbsp;Natchiappan Senthilkumar,&nbsp;Shanmugam Velayuthaprabhu,&nbsp;Muthukrishnan Saradhadevi,&nbsp;Palanisamy Sampathkumar,&nbsp;Arumugam Vijaya Anand","doi":"10.1155/2022/2238320","DOIUrl":"https://doi.org/10.1155/2022/2238320","url":null,"abstract":"<p><strong>Background: </strong>Anemia is one of the predominant hematological conditions, whereas chronic obstructive pulmonary disease (COPD) is a predominant respiratory disease. These two diseases were found to be interlinked, but the physiological pathways are still unclear.</p><p><strong>Aim: </strong>The current study has been aimed at analysing the genetic interrelationship between anemia and COPD in accordance with different altitudes. <i>Methodology</i>. The genetic analysis was performed in the <i>SERPINA1</i> gene of anemia, COPD, and healthy individuals for the analysis of single nucleotide polymorphism at rs28949274 and rs17580 locations. <i>Result and Discussion</i>. The single nucleotide polymorphism at the locations rs28949274 and rs17580 was present in both anemic and COPD patients. The COPD patients were more prone to mutations (63% had rs28949274, and 11% had rs17580 polymorphisms) than the anemic patients (40% had rs28949274, and 1% had rs17580 polymorphisms). On the basis of altitude, high-altitude individuals were found to be more susceptible to both the polymorphisms.</p><p><strong>Conclusion: </strong>Based on the current findings, we suggest that the <i>SERPINA1</i> gene has a positive correlation with anemia as well as COPD, and the increase in altitude also influences the diseased conditions in a positive manner.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"2238320"},"PeriodicalIF":2.9,"publicationDate":"2022-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9592209/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40438661","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}

{"title":"Eplerenone Prevents Cardiac Fibrosis by Inhibiting Angiogenesis in Unilateral Urinary Obstruction Rats.","authors":"Yi Chang,&nbsp;Ying Ben,&nbsp;Hui Li,&nbsp;Yunzhao Xiong,&nbsp;Gege Chen,&nbsp;Juan Hao,&nbsp;Xuelian Ma,&nbsp;Xiaomeng Gao,&nbsp;Panpan Qiang,&nbsp;Tatsuo Shimosawa,&nbsp;Xiangting Wang,&nbsp;Fan Yang,&nbsp;Qingyou Xu","doi":"10.1155/2022/1283729","DOIUrl":"https://doi.org/10.1155/2022/1283729","url":null,"abstract":"<p><strong>Introduction: </strong>Cardiovascular disease constitutes the leading cause of mortality in patients with chronic kidney disease (CKD), which is termed cardiorenal syndrome type 4 (CRS-4). Here, we report the development of pathological cardiac remodeling and fibrosis in unilateral urinary obstruction (UUO) rats.</p><p><strong>Methods: </strong>Hematoxylin and eosin (H&E) staining was performed to observe the pathology of myocardial tissue. The degree of myocardial tissue fibrosis was observed by Masson and Sirius red staining. Immunohistochemical staining was applied to detect the expression of CD34 and CD105 in myocardial tissue, and immunofluorescent staining was performed to examine the expression of CD34, collagen I/collagen III, and alpha smooth muscle actin (<i>α</i>-SMA). The expression of the signal pathway-related proteins vascular endothelial growth factor A (VEGFA), vascular endothelial growth factor receptor 2 (VEGFR2), nuclear factor <i>κ</i>B (NF-<i>κ</i>B), and interleukin (IL)-1<i>β</i> was tested by western blotting. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA levels of serum and glucocorticoid-inducible kinase (SGK)-1, NF-<i>κ</i>B, and interleukin-1<i>β</i> (IL-1<i>β</i>).</p><p><strong>Results: </strong>The results showed the development of pathological cardiac remodeling and cardiac dysfunction in UUO rats. Moreover, there was more angiogenesis and endothelial-mesenchymal transition (End-MT) in the UUO group, and these effects were inhibited by eplerenone.</p><p><strong>Conclusions: </strong>The results indicated that this cardiac fibrosis was associated with angiogenesis and that End-MT was related to aldosterone and mineralocorticoid receptor (MR) activation. Moreover, in association with the MR/IL-1<i>β</i>/VEGFA signaling pathway, early treatment with the MR antagonist eplerenone in rats with UUO-induced CKD may significantly attenuate MR activation and cardiac fibrosis.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"1283729"},"PeriodicalIF":2.9,"publicationDate":"2022-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9509279/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40390666","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}

{"title":"Sex Difference in MasR Expression and Functions in the Renal System.","authors":"Samira Choopani,&nbsp;Mehdi Nematbakhsh","doi":"10.1155/2022/1327839","DOIUrl":"https://doi.org/10.1155/2022/1327839","url":null,"abstract":"<p><p>Renin-angiotensin system (RAS), as a critical system for controlling body fluid and hemostasis, contains peptides and receptors, including angiotensin 1-7 (Ang 1-7) and Mas receptor (MasR). Ang 1-7 implements its function via MasR. Ang II is another peptide in RAS that performs its actions via two Ang II type 1 and 2 receptors (AT1R and AT2R). The functions of AT2R and MasR are very similar, and both have a vasodilation effect, while AT1R has a vasoconstriction role. MasR affects many mechanisms in the brain, heart, blood vessels, kidney, lung, endocrine, reproductive, skeletal muscle, and liver and probably acts like a paracrine hormone in these organs. The effect of Ang 1-7 in the kidney is complex according to the hydroelectrolyte status, the renal sympathetic nervous system, and the activity level of the RAS. The MasR expression and function seem more complex than Ang II receptors and have interacted with Ang II receptors and many other factors, including sex hormones. Also, pathological conditions including hypertension, diabetes, and ischemia-reperfusion could change MasR expression and function. In this review, we consider the role of sex differences in MasR expression and functions in the renal system under physiological and pathological conditions.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"1327839"},"PeriodicalIF":2.9,"publicationDate":"2022-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9482541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33478244","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}

{"title":"Exploring the Impact of ACE Inhibition in Immunity and Disease.","authors":"Delia Oosthuizen,&nbsp;Edward D Sturrock","doi":"10.1155/2022/9028969","DOIUrl":"https://doi.org/10.1155/2022/9028969","url":null,"abstract":"<p><p>Angiotensin-converting enzyme (ACE) is a zinc-dependent dipeptidyl carboxypeptidase and is crucial in the renin-angiotensin-aldosterone system (RAAS) but also implicated in immune regulation. Intrinsic ACE has been detected in several immune cell populations, including macrophages and neutrophils, where its overexpression results in enhanced bactericidal and antitumour responses, independent of angiotensin II. With roles in antigen presentation and inflammation, the impact of ACE inhibitors must be explored to understand how ACE inhibition may impact our ability to clear infections or malignancy, particularly in the wake of the coronavirus (SARS-CoV2) pandemic and as antibiotic resistance grows. Patients using ACE inhibitors may be more at risk of postsurgical complications as ACE inhibition in human neutrophils results in decreased ROS and phagocytosis whilst angiotensin receptor blockers (ARBs) have no effect. In contrast, ACE is also elevated in certain autoimmune diseases such as rheumatoid arthritis and lupus, and its inhibition benefits patient outcome where inflammatory immune cells are overactive. Although the ACE autoimmune landscape is changing, some studies have conflicting results and require further input. This review seeks to highlight the need for further research covering ACE inhibitor therapeutics and their potential role in improving autoimmune conditions, cancer, or how they may contribute to immunocompromise during infection and neurodegenerative diseases. Understanding ACE inhibition in immune cells is a developing field that will alter how ACE inhibitors are designed in future and aid in developing therapeutic interventions.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"9028969"},"PeriodicalIF":2.9,"publicationDate":"2022-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9371878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33437719","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}

{"title":"Estradiol Supplement or Induced Hypertension May Attenuate the Angiotensin II Type 1 Receptor Antagonist-Promoted Renal Blood Flow Response to Graded Angiotensin II Administration in Ovariectomized Rats.","authors":"Samira Choopani,&nbsp;Mehdi Nematbakhsh","doi":"10.1155/2022/3223008","DOIUrl":"https://doi.org/10.1155/2022/3223008","url":null,"abstract":"<p><strong>Backgrounds: </strong>Estrogen replacement therapy (ERT) and hypertension may influence females' renin-angiotensin system (RAS) and its components. The angiotensin II (Ang II) type 1 receptor (AT1R) antagonist (losartan) may promote renal blood flow (RBF), and it is widely used in the clinic to control hypertension. The main objective of this study was the effects of estradiol or induced hypertension on RBF response to Ang II in losartan-treated ovariectomized (OVX) rats.</p><p><strong>Methods: </strong>Two groups of OVX rats were treated with placebo (group 1) and estradiol (group 2) for period of four weeks, and another group of OVX rats was subjected to induce hypertension by two-kidney one clip (2K1C) model (group 3). All the groups were subjected to the surgical procedure under anesthesia, and AT1R was blocked by losartan. RBF and renal vascular resistance (RVR) responses to Ang II administration were determined and compared.</p><p><strong>Results: </strong>Mean arterial (MAP) and renal perfusion (RPP) pressures in group 3 and uterus weight (UT) in group 2 were significantly more than other groups (<i>P</i> < 0.05). Ang II infusion resulted in dose-related percentage change increase in RBF and decrease in RVR. However, these responses in the OVX-estradiol and OVX-hypertensive rats were significantly lower than in the OVX-control group (<i>P</i> < 0.05). For instance, at the dose of 1000 ng/kg/min of Ang II administration, the percentage change of RBF was 45.1 ± 10.4%, 17.9 ± 2.3%, and 16.7 ± 4.7% in the groups of 1 to 3, respectively.</p><p><strong>Conclusion: </strong>Losartan prescription in some conditions such as hypertension or ERT could worsen RBF and RVR responses to Ang II.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"3223008"},"PeriodicalIF":2.9,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9270140/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40621528","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}

{"title":"The Effect of the Angiotensin-Converting Enzyme Inhibitor on Bone Health in Castrated Hypertensive Rats Is Mediated via the Kinin-Kallikrein System.","authors":"Na Zhang,&nbsp;Yanan Huo,&nbsp;Chen Yao,&nbsp;Jie Sun,&nbsp;Yafeng Zhang","doi":"10.1155/2022/9067167","DOIUrl":"https://doi.org/10.1155/2022/9067167","url":null,"abstract":"<p><strong>Background: </strong>In previous studies, angiotensin-converting enzyme inhibitor (ACEI) use was associated with increased bone loss, while an angiotensin II type I receptor blocker had no effect on bone loss in elder subjects, which suggested that the effect of ACEI on bone loss was not mediated through the classical renin-angiotensin system. In this study, we set to investigate whether the effect of ACEI on bone deterioration was mediated via the kinin-kallikrein system.</p><p><strong>Methods: </strong>Six-month-old male and female spontaneously hypertensive rats were used. The effect of captopril on blood pressure, serum Ang II, and bradykinin concentration was measured in intact rats. Ovariectomy and orchidectomy were performed to establish an osteoporosis model in female and male rats, respectively. Captopril and the bradykinin receptor blocker icatibant (HOE140) were administered after operation for 12 weeks. Serum Ang II and bradykinin concentration, bone turnover markers, bone mineral density (BMD), and bone microarchitecture were evaluated. Femur samples were subjected to a mechanical test.</p><p><strong>Results: </strong>Captopril decreased blood pressure and serum Ang II concentration and increased serum bradykinin concentration in intact rats (<i>P</i> < 0.05). After castration, captopril decreased serum Ang II concentration (<i>P</i> < 0.05); in female rats, icatibant increased serum Ang II concentration (<i>P</i> < 0.05). Captopril increased serum bradykinin concentration (<i>P</i> < 0.05); in male rats, icatibant decreased serum bradykinin concentration (<i>P</i> < 0.05). Captopril increased the rat urine deoxypyridinoline-creatinine ratio (DPD/Cr) and serum osteocalcin concentration (<i>P</i> < 0.05). Icatibant decreased urine DPD/Cr in male rats (<i>P</i> < 0.05) and increased osteocalcin concentration in female rats (<i>P</i> < 0.05). Captopril increased cancellous BMD in castrated hypertensive rats (<i>P</i> < 0.05), and icatibant further increased cancellous BMD (<i>P</i> < 0.05), which was due to the increased trabecular bone number. In mechanical testing, ACEI increased bone strength (<i>P</i> < 0.05), and icatibant further improved it (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>ACEI decreased bone deterioration in both male and female hypertensive rats, and the bradykinin receptor blocker further decreased bone deterioration.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"9067167"},"PeriodicalIF":2.9,"publicationDate":"2022-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9213206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40582293","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}

{"title":"Associations between AGT M235T Polymorphism and Cancer: An Updated Meta-Analysis.","authors":"Junyan Kou,&nbsp;Jing Huang","doi":"10.1155/2022/7862709","DOIUrl":"https://doi.org/10.1155/2022/7862709","url":null,"abstract":"<p><p>We assessed the relationship between AGT gene M235T polymorphism and the susceptibility to cancer by performing an updated meta-analysis. This study retrospectively searched related articles in the electronic databases. Afterwards, we determined combined odds ratios (ORs) and related 95% confidence intervals (CIs) by the fixed- or random-effects model. The present meta-analysis enrolled altogether 9 articles. On the whole, the relationship between AGT M235T polymorphism and the cancer risk was not significant among the entire population (TT vs. MM: OR = 1.28, 95%CI = 0.80 - 2.04; TM vs. MM: OR = 0.90, 95%CI = 0.53 - 1.52; recessive model: OR = 1.13, 95%CI = 0.83 - 1.52; dominant model: OR = 0.93, 95%CI = 0.55 - 1.57). Subgroup analysis by ethnicity, cancer type, and study quality for the relationship between the AGT M235T polymorphism and cancer risk showed no significant association. According to findings in the present meta-analysis, AGT M235T polymorphism may not be related to cancer susceptibility.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"7862709"},"PeriodicalIF":2.9,"publicationDate":"2022-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8916873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40314391","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}

{"title":"Ocular Distribution of the Renin-Angiotensin-Aldosterone System in the Context of the SARS-CoV-2 Pandemic.","authors":"Ali Abid,&nbsp;Muhammad Azaan Khan,&nbsp;Brendon Lee,&nbsp;Andrew White,&nbsp;Nicole Carnt,&nbsp;Sana Arshad,&nbsp;Chameen Samarawickrama","doi":"10.1155/2022/9970922","DOIUrl":"https://doi.org/10.1155/2022/9970922","url":null,"abstract":"<p><p>The COVID-19 pandemic has resulted in an unprecedented impact on global health, economy, and way of life. SARS-CoV-2, the virus responsible for the disease, utilizes the ACE2 receptor found on host cells to mediate entry, replication, and infection. Numerous studies have elucidated the presence of many components of the renin-angiotensin-aldosterone system (RAAS) in the eye, including the ACE2 receptor. Considering this, and the anatomical vulnerability that the exposed ocular surface offers with its interconnectedness to the respiratory system, there is a theoretical risk of pathogen entry from the ocular route as well as the development of COVID-19-associated eye disease. Despite this, the actual epidemiological data demonstrates low ocular symptoms, possibly due to differing ACE2 receptor expression across age, ethnicity, and sex coupled with the protective properties of tears. We summarize the current literature on ocular RAAS with specific focus on the ACE2 receptor and its interplay with the SARS-CoV-2 virus.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"9970922"},"PeriodicalIF":2.9,"publicationDate":"2022-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8831072/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39929578","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}

{"title":"Role and Mechanism of the Renin-Angiotensin-Aldosterone System in the Onset and Development of Cardiorenal Syndrome.","authors":"Kexin Ma,&nbsp;Weifang Gao,&nbsp;Huazhou Xu,&nbsp;Wenjie Liang,&nbsp;Guoping Ma","doi":"10.1155/2022/3239057","DOIUrl":"https://doi.org/10.1155/2022/3239057","url":null,"abstract":"<p><p>Cardiorenal syndrome (CRS), a clinical syndrome involving multiple pathological mechanisms, exhibits high morbidity and mortality. According to the primary activity of the disease, CRS can be divided into cardiorenal syndrome (type I and type II), renal heart syndrome (type III and type IV), and secondary heart and kidney disease (type V). The renin-angiotensin-aldosterone system (RAAS) is an important humoral regulatory system of the body that exists widely in various tissues and organs. As a compensatory mechanism, the RAAS is typically activated to participate in the regulation of target organ function. RAAS activation plays a key role in the pathogenesis of CRS. The RAAS induces the onset and development of CRS by mediating oxidative stress, uremic toxin overload, and asymmetric dimethylarginine production. Research on the mechanism of RAAS-induced CRS can provide multiple intervention methods that are of great significance for reducing end-stage organ damage and further improving the quality of life of patients with CRS.</p>","PeriodicalId":520698,"journal":{"name":"Journal of the renin-angiotensin-aldosterone system : JRAAS","volume":" ","pages":"3239057"},"PeriodicalIF":2.9,"publicationDate":"2022-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8803448/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39882554","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}