Journal of the Renin-Angiotensin-Aldosterone System

Objective. Coronary artery disease (CAD), one of the commonest cardiovascular diseases, has high morbidity and mortality. Absent in melanoma 2 (AIM2) is involved in atherosclerosis, and no clinical trials have explored the association between AIM2 and CAD. Therefore, this study was aimed at evaluating the predictive and short-term prognostic value of AIM2 for CAD. Methods. 279 patients who underwent coronary angiography were enrolled in this study. The AIM2 level was detected from the serum of collected artery blood samples. The association of serum AIM2 level with the prediction and short-term prognosis of CAD was further assessed. Results. The serum AIM2 level of the CAD group was significantly higher than the control group ( vs. ; ). AIM2 was demonstrated to be the risk factor of CAD [odds ratio, 1.589; 95% confidence interval (CI), 1.346-1.876; ]. The area under the receiver operating characteristic (ROC) curve of 0.738 showed the diagnostic value of AIM2 in CAD. Additionally, AIM2 was an independent predictor of major adverse cardiovascular events (hazard ratio, 1.453; 95% CI, 1.086-1.945; ), and CAD patients with high AIM2 levels (>4.9 ng/mL) had a markedly lower survival rate (log-rank ). Conclusions. The serum AIM2  ng/mL can predict CAD to a certain extent. AIM2 might be an independent predictor of its short-term poor prognosis.

Coronavirus disease 2019 (COVID-19) is an illness caused by a novel coronavirus called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Mutations in the genetic coding and the variations in the spike proteins are critical for the virus’s mechanism of facilitating fusion with the human host, making the disease more severe. Recent research indicates that comorbidities including diabetes, hypertension, renal disease, heart failure, and atherosclerosis play a significant role in the severity and high mortality rates of (COVID-19), suggesting that perhaps the metabolic syndrome and its components are associated with COVID-19 morbidity. Primarily, angiotensin-converting enzyme 2 (ACE2) receptor is identified as the entrance receptor of SARS-CoV-2. Increased ACE2 expression, endothelial dysfunction plays a vital role in the progression and severity of complications developed due to COVID-19. In this review, we will discuss the association and management of cardiorenal disease and COVID-19.

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: , ; TM vs. MM: , ; recessive model: , ; dominant model: , ). 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.

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.

Objective. Contrast-induced acute kidney injury (CI-AKI) is a serious side effect of contrast media use. The purpose of this study was to investigate the role and mechanism of tolvaptan (TOL) in CI-AKI. Methods. 24 Wistar male rats were randomly divided into 4 groups (). And a rat model of CI-AKI was established. Then, the blood and urine of rats in each group were collected to detect relevant parameters. HE staining was utilized for the observation of the pathological changes of rat kidney tissues, TUNEL assay for the detection of tubular cell apoptosis, biochemical detection for the confirmation of oxidative stress level in kidney tissues, and western blot for the test of the expression of apoptotic proteins and the Nrf2 signaling pathway-related proteins in kidney tissues. Results. TOL could significantly reduce the serum level of urea nitrogen, creatinine, and neutrophil gelatinase-associated lipocalin and decrease serum Cys-C and urine KIM-1 in CI-AKI rats. The result above meant that TOL could improve kidney injury and reduce tubular cell apoptosis in CI-AKI rats. In addition, TOL contributed to a reduction of oxidative stress level by downregulating myeloperoxidase level and increasing the activities of superoxide dismutase and glutathione peroxidase in the kidney tissue of CI-AKI rats. After the pretreatment of TOL, the expression of proapoptotic proteins cleaved-caspase 3 and BAX, as well as mitochondrial fusion proteins DRP1 and MFN2 was downregulated, while the expression of Bcl-2 and PINK1 was upregulated in the kidney tissue of CI-AKI rats. Further, TOL could activate the Nrf2 signaling pathway, and the Nrf2 inhibitor ML385 reversed the effect of TOL on CI-AKI. Conclusion. TOL can improve CI-AKI by activating the Nrf2/HO-1 signaling pathway, inhibiting oxidative stress response, and reducing tubular cell apoptosis.

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.