U-Shaped Relationship between Sleep Duration and CKD in US Adults: Data from National Health and Nutrition Examination Survey (NHANES) 2005-2014.

INTRODUCTION: Short and long sleep durations have been associated with adverse health outcomes. The objective of this study was to examine the association between self-reported sleep duration and chronic kidney disease (CKD) in the general population on the basis of the National Health and Nutrition Examination Survey (NHANES) database. METHODS: A total of 28,239 adults aged ≥18 years who participated in the 2005-2014 NHANES were analyzed. CKD was defined as an estimated glomerular filtration rate <60 mL/min per 1.73 m2 or urinary albumin/urine creatinine ratio ≥300 mg/g. Very short sleepers and short sleepers were defined as those who sleep ≤5 h or 5.1-6.9 h per day, respectively. Long sleepers and very long sleepers were defined as those who sleep 9.0-10.9 h or ≥11 h per day, respectively. Normal sleepers were defined as those who sleep 7.0-8.9 h. The association between sleep duration and CKD was assessed using a logistic regression model. RESULTS: Very short (≤5 h) sleep duration was associated with higher odds of CKD (multiadjusted OR, 1.38; 95% confidence interval, 1.17-1.62 comparing normal categories of 7.0-8.9 h; P trend = 0.01), after adjusting for potential confounders. Participants with long (9-10.9 h) sleep duration also tended to have a higher odds of CKD (multiadjusted OR, 1.39; 95% confidence interval, 1.20-1.61 comparing normal categories of 7.0-8.9 h; P trend = 0.01). This risk was further increased in those whose sleep duration exceeded 11 h (multiadjusted OR, 2.35; 95% confidence interval, 1.64-3.37 comparing normal categories of 7.0-8.9; P trend = 0.01). However, there was no statistically significant association between short (≤6.0-7.9 h) sleep duration and CKD (multiadjusted OR, 1.05; 95% confidence interval, 0.96-1.14 comparing normal categories of 7.0-8.9 h; P trend = 0.32). CONCLUSION: We demonstrated that the higher CKD prevalence estimates were found in very short (≤5 h) and long (9.0-10.9 h) sleep durations in an apparently healthy population aged ≥18 years in the USA. This prevalence of CKD is further increased in those whose sleep duration exceeds 11 h. Our cross-sectional analyses clarified the U-shaped temporal relationship between sleep duration and CKD.

The value of urinary interleukin-18 in predicting acute kidney injury: a systematic review and meta-analysis.

AIMS: The aim of this study was to systematically review relevant studies to evaluate the value of urinary interleukin-18 (uIL-18) in predicting acute kidney injury (AKI). METHODS: A comprehensive search of PubMed, Medline, Embase, and Cochrane Library was conducted for literature published up to 1 August 2022. Quality Assessment Tool for Diagnostic Accuracy Studies-2 (QUADAS-2) was applied to assess the literature quality. Then, relevant data were extracted from each eligible study and a random-effects regression model was utilized to pool sensitivity, specificity, and construct summary receiver operating characteristic (SROC) and area under curve (AUC). RESULTS: Twenty-six studies with 7183 patients were enrolled and relevant information was extracted. The estimated sensitivity and specificity of uIL-18 in the diagnosis of AKI were 0.64 (95% confidence interval (CI): 0.54-0.73) and 0.77 (95%CI: 0.71-0.83), respectively. The pooled diagnostic odds ratio (DOR) was 6.08 (95%CI: 3.63-10.18), and the AUC of uIL-18 in predicting AKI was 0.78 (95%CI: 0.74-0.81). Subgroup analysis showed that uIL-18 in pediatric patients was more effective in predicting AKI than in adults (DOR: 7.33 versus 5.75; AUC: 0.81 versus 0.77). CONCLUSIONS: Urinary IL-18 could be a relatively good biomarker with moderate predictive value for AKI, especially in pediatric patients. However, further research and clinical settings are still needed to validate our findings.

Emerging therapeutic strategies targeting extracellular histones for critical and inflammatory diseases: an updated narrative review.

Extracellular histones are crucial damage-associated molecular patterns involved in the development and progression of multiple critical and inflammatory diseases, such as sepsis, pancreatitis, trauma, acute liver failure, acute respiratory distress syndrome, vasculitis and arthritis. During the past decade, the physiopathologic mechanisms of histone-mediated hyperinflammation, endothelial dysfunction, coagulation activation, neuroimmune injury and organ dysfunction in diseases have been systematically elucidated. Emerging preclinical evidence further shows that anti-histone strategies with either their neutralizers (heparin, heparinoids, nature plasma proteins, small anion molecules and nanomedicines, etc.) or extracorporeal blood purification techniques can significantly alleviate histone-induced deleterious effects, and thus improve the outcomes of histone-related critical and inflammatory animal models. However, a systemic evaluation of the efficacy and safety of these histone-targeting therapeutic strategies is currently lacking. In this review, we first update our latest understanding of the underlying molecular mechanisms of histone-induced hyperinflammation, endothelial dysfunction, coagulopathy, and organ dysfunction. Then, we summarize the latest advances in histone-targeting therapy strategies with heparin, anti-histone antibodies, histone-binding proteins or molecules, and histone-affinity hemoadsorption in pre-clinical studies. Finally, challenges and future perspectives for improving the clinical translation of histone-targeting therapeutic strategies are also discussed to promote better management of patients with histone-related diseases.

The association between visceral adiposity index and decreased renal function: A population-based study.

Aims: We aimed to investigate the association of visceral adiposity index (VAI) with decreased renal function in US adults. Design and methods: Cross-sectional data were analyzed for 35,018 adults in the National Health and Nutrition Examination Survey (NHANES) 2005-2018. VAI was determined using waist circumference, body mass index (BMI), triglycerides (TGs) and high-density lipoprotein-cholesterol. Albuminuria was defined as urinary albumin-to-creatinine ratio (ACR) >30 mg/g. A low estimated-glomerular filtration rate (eGFR) was defined as an eGFR lower than 60 ml/min/1.73 m2. Chronic kidney disease (CKD) was defined as either albuminuria or low-eGFR. A multivariable logistic regression analysis was utilized to explore the relationship of VAI with albuminuria, low-eGFR and CKD. Subgroup analysis and interaction tests were also conducted. Results: A total of 35,018 participants were enrolled with albuminuria, low-eGFR, and CKD prevalence rates of 5.18, 6.42, and 10.62%, respectively, which increased with the higher VAI tertiles. After full adjustment, a positive association of VAI with albuminuria (OR = 1.03, 95% CI: 1.00, 1.06) and CKD (OR = 1.04, 95% CI: 1.02, 1.06) was observed. Participants in the highest VAI tertile had a significantly 30% increased risk for albuminuria (OR = 1.30, 95% CI: 1.07, 1.58) and a 27% increased risk for CKD (OR = 1.27, 95% CI: 1.08, 1.49) compared with those in the lowest VAI tertile. No statistically significant association between VAI and low-eGFR was detected. Subgroup analysis and the interaction term indicated that there was no significant difference among different stratifications. Conclusion: Visceral adiposity accumulation evaluating by VAI was associated with increased likelihood of the decline in renal function.

NOX4 is a potential therapeutic target in septic acute kidney injury by inhibiting mitochondrial dysfunction and inflammation.

Rationale: Sepsis is a severe clinical syndrome featured through organ dysfunction due to infection, while the accompanying acute kidney injury (AKI) is linked to significant incidence of morbidity as well as mortality. Recently, emerging evidence has revealed that nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4) is implicated in various renal diseases, while its role and modulation in septic acute kidney injury (S-AKI) remains largely unknown. Methods: In vivo, S-AKI in wild-type and renal tubular epithelial cell (RTEC)-specific NOX4 knockout mice was induced by lipopolysaccharides (LPS) injection or cecal ligation and puncture (CLP). In vitro, TCMK-1 (mouse kidney tubular epithelium cell line) cells were treated with LPS. Serum and supernatant biochemical, mitochondrial dysfunctional, inflammatory and apoptotic parameters were measured and compared across groups. The activation of reactive oxygen species (ROS) and NF-κB signaling was also assessed. Results: NOX4 was predominantly upregulated in RTECs of S-AKI mouse model induced by LPS/CLP and cultured TCMK-1 cells exposed to LPS. RTEC-specific deletion of NOX4 or pharmacological inhibition of NOX4 by GKT137831 both alleviated LPS/CLP-injured renal function and pathology in mice. Furthermore, NOX4 inhibition alleviated mitochondrial dysfunction supported by ultrastructural damage, reduction of ATP production and mitochondrial dynamics imbalance, together with inflammation and apoptosis in kidney injured by LPS/CLP and TCMK-1 cells injured by LPS, while NOX4 overexpression aggravated the above-mentioned indices in TCMK-1 cells with LPS stimulation. Mechanism-wise, the raised NOX4 in RTECs may induce ROS and NF-κB signaling activation in S-AKI. Conclusions: Collectively, genetic or pharmacological inhibition of NOX4 protects from S-AKI by reducing generation of ROS and activation of NF-κB signal, which suppress mitochondrial dysfunction, inflammation together with apoptosis. NOX4 may act as a novel target for the S-AKI therapy.

Effects of Expanded Hemodialysis with Medium Cut-Off Membranes on Maintenance Hemodialysis Patients: A Review.

Kidney failure is associated with high morbidity and mortality. Hemodialysis, the most prevalent modality of renal replacement therapy, uses the principle of semipermeable membranes to remove solutes and water in the plasma of patients with kidney failure. With the evolution of hemodialysis technology over the last half century, the clearance of small water-soluble molecules in such patients is adequate. However, middle molecules uremic toxins are still retained in the plasma and cause cardiovascular events, anemia, and malnutrition, which significantly contribute to poor quality of life and high mortality in maintenance hemodialysis patients. A new class of membrane, defined as a medium cut-off (MCO) membrane, has emerged in recent years. Expanded hemodialysis with MCO membranes is now recognized as the artificial kidney model closest to natural kidney physiology. This review summarizes the unique morphological characteristics and internal filtration-backfiltration mechanism of MCO membranes, and describes their effects on removing uremic toxins, alleviating inflammation and cardiovascular risk, and improving quality of life in maintenance hemodialysis patients.

Higher visceral adiposity index is associated with increased likelihood of abdominal aortic calcification.

BACKGROUND: The negative effects of visceral adiposity accumulation on cardiovascular health have drawn much attention. However, the association between the Visceral Adiposity Index (VAI) and Abdominal Aortic Calcification (AAC) has never been reported before. The authors aimed to investigate the association between the VAI and AAC in US adults. METHODS: Cross-sectional data were derived from the 2013 to 2014 National Health and Nutrition Examination Survey (NHANES) of participants with complete data of VAI and AAC scores. Weighted multivariable regression and logistic regression analysis were conducted to explore the independent relationship between VAI and AAC. Subgroup analysis and interaction tests were also performed. RESULTS: A total of 2958 participants were enrolled and participants in the higher VAI tertile tended to have a higher mean AAC score and prevalence of severe AAC. In the fully adjusted model, a positive association between VAI and AAC score and severe AAC was observed (ß = 0.04, 95% CI 0.01‒0.08; OR = 1.04, 95% CI 1.01‒1.07). Participants in the highest VAI tertile had a 0.41-unit higher AAC score (ß = 0.41, 95% CI 0.08‒0.73) and a significantly 68% higher risk of severe AAC than those in the lowest VAI tertile (OR = 1.68, 95% CI 1.04‒2.71). Subgroup analysis and interaction tests indicated that there was no dependence for the association of VAI and AAC. CONCLUSION: Visceral adiposity accumulation evaluated by the VAI was associated with a higher AAC score and an increased likelihood of severe AAC.

Exosomal STAT1 derived from high phosphorus­stimulated vascular endothelial cells induces vascular smooth muscle cell calcification via the Wnt/ß­catenin signaling pathway.

Vascular calcification is commonly observed in chronic kidney disease. The mechanism of how the calcification signal from endothelial cells is transmitted to vascular smooth muscle cells (VSMCs) remains unknown. The aim of the present study was to investigate whether exosomes from HUVECs (HUVEC­Exos) could regulate VSMC calcification and its potential signaling pathway. HUVEC­Exos were isolated from HUVECs under no phosphorus (NP) and high phosphorus (HP) conditions. Alizarin Red S staining and calcium (Ca) content analysis were carried out to detect calcification in VSMCs. Proteomics analysis was carried out to detect the differential expression of exosomal proteins. Protein and mRNA levels were measured by western blot analysis and reverse transcription­quantitative PCR (RT­qPCR). Exosomes derived from HP­HUVECs promoted the calcification of VSMCs, as assessed by Alizarin Red S staining, alkaline phosphatase activity assays, Ca content measurements and the increased expression of runt­related transcription factor 2 and osteopontin. Proteomic analysis detected the upregulation of STAT1 in HP­exosomes from HUVECs (HUVEC­Exos) compared with NP­HUVEC­Exos, which was also confirmed by western blot analysis and RT­qPCR. Inhibition of STAT1 expression in VSMCs using fludarabine or knockdown of STAT1 expression using small interfering RNA alleviated the calcification of VSMCs. Furthermore, lithium chloride (Wnt activator) reversed the protective effect of STAT1 inhibition on VSMC calcification, while Dickkopf­1 (Wnt inhibitor) exerted the opposite effect, suggesting that activation of the Wnt/ß­catenin signaling pathway was involved in STAT1­mediated VSMC calcification. In conclusion, the present results indicated that exosomal STAT1 derived from HP­treated HUVECs could promote VSMC calcification, and activation of the Wnt/ß­catenin pathway may be a potential mechanism of the VSMC calcification promoted by exosomes.

Resolvin D1 attenuates sepsis induced acute kidney injury targeting mitochondria and NF-κB signaling pathway.

Background: Acute kidney injury is a highly common and multifactorial renal disease resulting in significant morbidity and mortality, especially sepsis-induced acute kidney injury. There is no effective therapy available to treat or prevent sepsis-induced acute kidney injury. One of the specialized pro-resolving mediators, Resolvin D1 exhibits special anti-inflammatory effects in several inflammatory disease models, but there is little evidence about the effect and mechanism of Resolvin D1 in sepsis-induced acute kidney injury. Methods: We conducted experiments to explore the effect and mechanism of Resolvin D1 in sepsis-induced acute kidney injury. In vitro, human proximal tubular epithelial cells were used to test the apoptosis ratio, cell viability and reactive oxygen species level. In vivo, C57BL/6 mice were injected with lipopolysaccharide to establish a sepsis-induced acute kidney injury model. Renal function and structure, apoptosis ratio of kidney cells, mitochondrial structure and function and related protein and gene levels were assessed. Results: In vitro, the resolvin D1-treated group showed higher cell viability and lower reactive oxygen species levels and apoptosis ratios than the LPS group. In vivo, Resolvin D1 can not only improve renal function and mitochondrial function but also reduce the apoptosis ratio, while mediating mitochondrial dynamics and inhibiting NF-κB pathway. Conclusions: Resolvin D1 has a good renoprotective effect by maintaining mitochondrial dynamics and inhibiting the NF-κB pathway.

Effect of Anticoagulant Administration on the Mortality of Hospitalized Patients With COVID-19: An Updated Systematic Review and Meta-Analysis.

Background: Anticoagulation is generally used in hospitalized patients with coronavirus disease 2019 (COVID-19) as thromboprophylaxis. However, results from different studies comparing the effect of anticoagulation on the mortality of COVID-19 patients with non-anticoagulation are inconclusive. Methods: Our systematic review included observational trials if they studied anticoagulant therapy in hospitalized patients with COVID-19 for mortality or bleeding events. Dichotomous variables from individual studies were pooled by risk ratio (RR) and their 95% confidence interval (95% CI) using the random-effects model. Grading of Recommendations Assessment, Development and Evaluation was used to assess the quality of evidence. Results: A total of 11 observational studies enrolling 20,748 hospitalized COVID-19 patients overall were included. A pooled meta-analysis of these studies showed that anticoagulation therapy, compared with non-anticoagulation therapy, was associated with lower mortality risk (RR 0.70, 95% CI 0.52-0.93, p = 0.01). The evidence of benefit was stronger among critically ill COVID-19 patients in the intensive care units (RR 0.59, 95% CI 0.43-0.83, p = 0.002). Additionally, severe bleeding events were not associated with the administration of anticoagulants (RR 0.93, 95% CI 0.71-1.23, p = 0.63). Conclusion: Among patients with COVID-19 admitted to hospital, the administration of anticoagulants was associated with a decreased mortality without increasing the incidence of bleeding events.

The Association Between Dietary Inflammatory Potential and Sex Hormones in Male Children and Adolescents Aged 6-19 Years.

Aims: This study aimed to assess the relationship between dietary inflammatory index (DII) and sex hormones in male children and adolescents aged 6-19 years. Methods: We obtained data from the 2013-2016 National Health and Nutrition Examination Survey (NHANES). Male participants aged 6-19 years old with the complete data of DII and sex hormones were included. Weighted multiple regression analysis and subgroup analysis were preformed to estimate the independent relationship between DII and sex hormones. Results: A total of 1717 male participants with the average age of 13.02 ± 3.82 years were enrolled, of whom 41.3% (n=713) were children and 58.47% (n=1004) were adolescents. In children, mean DII was 0.18 ± 1.67, with scores ranging from -4.53 to 4.08. As for adolescents, the mean DII was 0.36 ± 1.98, mean total testosterone (TT) was 376.94 ± 206.69 ng/dl overall. A negative association between DII with TT and estradiol (E2) was observed (TT: ß=-11.97, P=0.0006; E2: ß=-0.45, P=0.0108) in male adolescent. Subgroup analysis and interaction test results indicated that this association was similar in male adolescents with different body mass index. No statistically significant association was observed in children. Conclusions: Pro-inflammatory diet was associated with lower TT and E2 level in male adolescent, while no association with statistical significance between them was observed in male children. However, more studies are still needed to validate the causal relationship between DII and sex hormones.

Greater Dietary Inflammatory Potential Is Associated With Higher Likelihood of Abdominal Aortic Calcification.

Aims: We aimed to assess the association between dietary inflammation index (DII) and abdominal aortic calcification (AAC) in US adults aged ≥40 years. Methods: Data were obtained from the 2013-2014 National Health and Nutrition Examination Survey (NHANES). Participants who were <40 years old and missing the data of DII and AAC were excluded. DII was calculated based on a 24-h dietary recall interview for each participant. AAC score was quantified by assessing lateral spine images and severe AAC was defined as AAC score >6. Weighted multivariable regression analysis and subgroup analysis were preformed to estimate the independent relationship between DII with AAC score and severe AAC. Results: A total of 2,897 participants were included with the mean DII of -0.17 ± 2.80 and the mean AAC score of 1.462 ± 3.290. The prevalence of severe AAC was 7.68% overall, and participants in higher DII quartile tended to have higher rates of severe AAC (Quartile 1: 5.03%, Quartile 2: 7.44%, Quartile 3: 8.38%, Quartile 4: 10.46%, p = 0.0016). A positive association between DII and AAC score was observed (ß = 0.055, 95% CI: 0.010, 0.101, p = 0.01649), and higher DII was associated with an increased risk of severe AAC (OR = 1.067, 95% CI: 1.004, 1.134, p = 0.03746). Subgroup analysis indicated that this positive association between DII and AAC was similar in population with differences in gender, age, BMI, hypertension status, and diabetes status and could be appropriate for different population settings. Conclusion: Higher pro-inflammatory diet was associated with higher AAC score and increased risk of severe AAC. Anti-inflammatory dietary management maybe beneficial to reduce the risk of AAC.

Maresin 1 Attenuates Lipopolysaccharide-Induced Acute Kidney Injury via Inhibiting NOX4/ROS/NF-κB Pathway.

Sepsis-associated acute kidney injury (S-AKI) is a common complication in hospitalized and critically ill patients, which increases the risk of multiple comorbidities and is associated with extremely high mortality. Maresin 1 (MaR1), a lipid mediator derived from the omega-3 fatty acid docosahexaenoic acid has been reported to protect against inflammation and promote the regression of acute inflammation. This study proposed to systematically investigate the renoprotective effects and potential molecular mechanism of MaR1 in septic acute kidney injury. We established a S-AKI animal model by a single intraperitoneal injection of lipopolysaccharide (LPS), 10 mg/kg, on male C57BL/6J mice. LPS-stimulated (100 µg/ml) mouse kidney tubular epithelium cells (TCMK-1) were used to simulate septic AKI in vitro. The results showed that pretreatment with MaR1 significantly reduced serum creatinine and blood urea nitrogen levels as well as tubular damage scores and injury marker neutrophil gelatinase-associated lipocalin in septic AKI mice. Meanwhile, MaR1 administration obviously diminished pro-inflammatory cytokines (TNF-α, IL-6, IL-1ß, and MCP-1), downregulated BAX and cleaved caspase-3 expression, and upregulated BCL-2 expression in the injured kidney tissues and TCMK-1 cells. In addition, MaR1 reduced malondialdehyde production and improved the superoxide dismutase activity of renal tissues while inhibiting reactive oxygen species (ROS) production and protecting the mitochondria. Mechanistically, LPS stimulated the expression of the NOX4/ROS/NF-κB p65 signaling pathway in S-AKI kidneys, while MaR1 effectively suppressed the activation of the corresponding pathway. In conclusion, MaR1 attenuated kidney inflammation, apoptosis, oxidative stress, and mitochondrial dysfunction to protect against LPS-induced septic AKI via inhibiting the NOX4/ROS/NF-κB p65 signaling pathway.

Circulating Histones in Sepsis: Potential Outcome Predictors and Therapeutic Targets.

Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection and is associated with high morbidity and mortality. Circulating histones (CHs), a group of damage-associated molecular pattern molecules mainly derived from neutrophil extracellular traps, play a crucial role in sepsis by mediating inflammation response, organ injury and death through Toll-like receptors or inflammasome pathways. Herein, we first elucidate the molecular mechanisms of histone-induced inflammation amplification, endothelium injury and cascade coagulation activation, and discuss the close correlation between elevated level of CHs and disease severity as well as mortality in patients with sepsis. Furthermore, current state-of-the-art on anti-histone therapy with antibodies, histone-binding proteins (namely recombinant thrombomodulin and activated protein C), and heparin is summarized to propose promising approaches for sepsis treatment.

Associations Between 25-Hydroxyvitamin D, Kidney Function, and Insulin Resistance Among Adults in the United States of America.

BACKGROUND: Although many molecular studies have tried to explore the relationship between vitamin D metabolism and kidney function, the association between 25-hydroxyvitamin D [25(OH)D] and kidney function is still controversial. Previous studies reported that low vitamin D status and decreased kidney function were associated with insulin resistance (IR). However, neither of them was confirmed by large population-based studies. This study evaluated the associations between 25(OH)D and kidney function and the associations between both of them and IR among adults in the United States of America (USA). METHODS: We analyzed 36,523 adults from the National Health and Nutrition Examination Survey (NHANES) (2001-2014). Kidney function was assessed by the estimated glomerular filtration rate (eGFR), and IR was assessed by homeostasis model assessment (HOMA-IR). All data were survey-weighted, and corresponding linear regression models were performed to examine the associations. RESULTS: The mean serum 25(OH)D levels were found to be increased in participants with decreased kidney function (eGFR <90 ml/min/1.73 m2), and each unit of decreased serum 25(OH)D concentrations predicted 0.453 ml/min/1.73 m2 (95% CI: 0.426 to 0.480, p < 0.0001) higher eGFR. In addition, each unit of decreased eGFR was associated with 0.007 higher HOMA-IR, while each unit of decreased 25(OH)D concentrations led to 0.025 higher HOMA-IR. CONCLUSIONS: Serum 25-hydroxyvitamin D concentrations were negatively associated with kidney function. IR appears in the early stage of kidney dysfunction, and both serum 25(OH)D concentrations and kidney function are negatively associated with IR. Clinicians should maintain appropriate serum 25(OH)D concentrations and doses of vitamin D supplements for different populations. The underlying mechanism of these associations still needs more research, especially the negative association between serum 25(OH)D concentrations and kidney function.

A narrative review of exosomes in vascular calcification.

Vascular calcification (VC) is the abnormal deposition of calcium, phosphorus, and other minerals in the vessel wall and can be commonly observed in diabetes, chronic kidney disease, and chronic inflammatory disease. It is closely associated with mortality from cardiovascular events. Traditionally, calcification is considered as a degenerative disease associated with the aging process, while increasing evidence has shown that the occurrence and development of calcification is an active biological process, which is highly regulated by multiple factors. The molecular mechanisms of VC have not yet been fully elucidated. Exosomes, as important transporters of substance transport and intercellular communication, have been shown to participate in VC. The regulation of VC by exosomes involves a number of complex biological processes, which occur through a variety of interaction mechanisms. However, the specific role and mechanism of exosomes in the process of VC are still not fully understood and require further study. This review will briefly describe the roles of exosomes in the process of VC including in the promotion of extracellular mineral deposits, induction of phenotypic conversion of vascular smooth muscle cells (VSMCs), transport of microRNA between cells, and regulation on autophagy and oxidative stress, with the aim of providing novel ideas for the clinical diagnosis and treatment of VC.

Higher visceral adiposity index is associated with increased likelihood of abdominal aortic calcification

Abstract Background: The negative effects of visceral adiposity accumulation on cardiovascular health have drawn much attention. However, the association between the Visceral Adiposity Index (VAI) and Abdominal Aortic Calcification (AAC) has never been reported before. The authors aimed to investigate the association between the VAI and AAC in US adults. Methods: Cross-sectional data were derived from the 2013 to 2014 National Health and Nutrition Examination Survey (NHANES) of participants with complete data of VAI and AAC scores. Weighted multivariable regression and logistic regression analysis were conducted to explore the independent relationship between VAI and AAC. Subgroup analysis and interaction tests were also performed. Results: A total of 2958 participants were enrolled and participants in the higher VAI tertile tended to have a higher mean AAC score and prevalence of severe AAC. In the fully adjusted model, a positive association between VAI and AAC score and severe AAC was observed (β = 0.04, 95% CI 0.01‒0.08; OR = 1.04, 95% CI 1.01‒1.07). Participants in the highest VAI tertile had a 0.41-unit higher AAC score (β = 0.41, 95% CI 0.08‒0.73) and a significantly 68% higher risk of severe AAC than those in the lowest VAI tertile (OR = 1.68, 95% CI 1.04‒2.71). Subgroup analysis and interaction tests indicated that there was no dependence for the association of VAI and AAC. Conclusion: Visceral adiposity accumulation evaluated by the VAI was associated with a higher AAC score and an increased likelihood of severe AAC.