GPX7 reduces chondrocyte inflammation and extracellular matrix degradation triggered by IL­1ß, via a mechanism mediated by ferroptosis.

During osteoarthritis (OA), chondrocytes become highly active, with increased matrix synthesis and inflammatory cytokine­induced catabolic pathways. Early intervention strategies targeting pathological changes may attenuate or halt disease progression. The present study aimed to reveal the role of glutathione peroxidase (GPX)7 in OA. For this purpose, a research model was established by inducing C28/I2 human chondrocytes with interleukin (IL)­1ß, and the expression level of GPX7 was determined. To explore its roles, C28/I2 cells were transfected to gain GPX7 overexpression. The effects of GPX7 overexpression on intracellular inflammation, extracellular matrix (ECM) degradation, apoptosis and ferroptosis were then evaluated. In addition, the cells were treated with the ferroptosis inducer, erastin, and its effects on the aforementioned phenotypes were assessed. The level of GPX7 was decreased in response to IL­1ß treatment, and GPX7 overexpression suppressed cellular inflammation, ECM degradation and apoptosis. Moreover, the reduction of lipid peroxidation, ferrous ions and transferrin indicated that GPX7 overexpression inhibited ferroptosis. Subsequently, inflammation, ECM degradation and apoptosis were found to be promoted in the cells upon treatment with erastin. These findings suggested that the regulatory role of GPX7 may be mediated by a pathway involving ferroptosis. On the whole, the present study revealed that GPX7 reduces IL­1ß­induced chondrocyte inflammation, apoptosis and ECM degradation partially through a mechanism involving ferroptosis. The results of the present study lay a theoretical foundation for subsequent OA­related research and may enable the development of translational strategies for the treatment of OA.

Circulating exosomal mir-16-2-3p is associated with coronary microvascular dysfunction in diabetes through regulating the fatty acid degradation of endothelial cells.

BACKGROUND: Coronary microvascular dysfunction (CMD) is a frequent complication of diabetes mellitus (DM) characterized by challenges in both diagnosis and intervention. Circulating levels of microRNAs are increasingly recognized as potential biomarkers for cardiovascular diseases. METHODS: Serum exosomes from patients with DM, DM with coronary microvascular dysfunction (DM-CMD) or DM with coronary artery disease (DM-CAD) were extracted for miRNA sequencing. The expression of miR-16-2-3p was assessed in high glucose-treated human aortic endothelial cells and human cardiac microvascular endothelial cells. Fluorescence in situ hybridization (FISH) was used to detect miR-16-2-3p within the myocardium of db/db mice. Intramyocardial injection of lentivirus overexpressing miR-16-2-3p was used to explore the function of the resulting gene in vivo. Bioinformatic analysis and in vitro assays were carried out to explore the downstream function and mechanism of miR-16-2-3p. Wound healing and tube formation assays were used to explore the effect of miR-16-2-3p on endothelial cell function. RESULTS: miR-16-2-3p was upregulated in circulating exosomes from DM-CMD, high glucose-treated human cardiac microvascular endothelial cells and the hearts of db/db mice. Cardiac miR-16-2-3p overexpression improved cardiac systolic and diastolic function and coronary microvascular reperfusion. In vitro experiments revealed that miR-16-2-3p could regulate fatty acid degradation in endothelial cells, and ACADM was identified as a potential downstream target. MiR-16-2-3p increased cell migration and tube formation in microvascular endothelial cells. CONCLUSIONS: Our findings suggest that circulating miR-16-2-3p may serve as a biomarker for individuals with DM-CMD. Additionally, miR-16-2-3p appears to alleviate coronary microvascular dysfunction in diabetes by modulating ACADM-mediated fatty acid degradation in endothelial cells.

Association between Body Fat Percentage and Cardiometabolic Diseases in General Population.

OBJECTIVES: The body fat percentage is an indicator of overall body fat related to metabolism and inflammation. Our study aims to analyze the association between body fat percentage and the risk of cardiometabolic diseases in the general population. METHODS: This was a retrospectively cross-sectional study. A total of 5084 participants enrolled from the National Health and Nutrition Examination Survey cycle of 1999-2004 were divided into quartiles according to their body fat percent levels. The body fat percentage was measured from bioelectrical impedance analysis. A history of cardiometabolic diseases, including cardiovascular disease, hypertension and diabetes mellitus, was ascertained from questionnaire, physical or laboratory examination. The association between body fat percentage and cardiometabolic diseases was investigated using multivariate logistic regression. RESULTS: Compared with the lowest quartile of body fat percentage, the multivariate-adjusted odds ratio and 95% confidence interval of the highest quartile was 3.99 (1.58-10.88) for cardiovascular disease, 1.08 (1.04-1.13) for hypertension and 3.08 (1.89-5.11) for diabetes. Body fat percentage independently increased the risk of cardiometabolic diseases as a continuous variable. CONCLUSIONS: Higher body fat percentage level was associated with a higher likelihood of cardiometabolic diseases, which could be a powerful predictive factor.

Ceria Nanozyme Coordination with Curcumin for Treatment of Sepsis-induced Cardiac Injury by Inhibiting Ferroptosis and Inflammation.

INTRODUCTION: Sepsis-induced cardiac injury is the leading cause of death in patients. Recent studies have reported that reactive oxygen species (ROS)-mediated ferroptosis and macrophage-induced inflammation are the two main key roles in the process of cardiac injury. The combination of ferroptosis and inflammation inhibition is a feasible strategy in the treatment of sepsis-induced cardiac injury. OBJECTIVES: In the present study, ceria nanozyme coordination with curcumin (CeCH) was designed by a self-assembled method with human serum albumin (HSA) to inhibit ferroptosis and inflammation of sepsis-induced cardiac injury. METHODS AND RESULTS: The formed CeCH obtained the superoxide dismutase (SOD)-like and catalase (CAT)-like activities from ceria nanozyme to scavenge ROS, which showed a protective effect on cardiomyocytes in vitro. Furthermore, it also showed ferroptosis inhibition to reverse cell death from RSL3-induced cardiomyocytes, denoted from curcumin. Due to the combination therapy of ceria nanozyme and curcumin, the formed CeCH NPs could also promote M2 macrophage polarization to reduce inflammation in vitro. In the lipopolysaccharide (LPS)-induced sepsis model, the CeCH NPs could effectively inhibit ferroptosis, reverse inflammation, and reduce the release of pro-inflammatory factors, which markedly alleviated the myocardial injury and recover the cardiac function. CONCLUSION: Overall, the simple self-assembled strategy with ceria nanozyme and curcumin showed a promising clinical application for sepsis-induced cardiac injury by inhibiting ferroptosis and inflammation. Acknowledgments: This study was supported by grants of the National Natural Science Foundation of China (82100398); the Nanjing Medical Science and Technique Development Foundation (YKK21068); Clinical Trials from the Affiliated Drum Tower Hospital, Medical School of Nanjing University (2023-LCYJ-PY-24); the Jiangsu Research Hospital Association for Precision Medication (JY202120); the Jiangsu Pharmaceutical Association for Jinpeiying Project (J2021001); China Postdoctoral Science Foundation (2022M721576).

Association between composite dietary antioxidant index and hypertension: insights from NHANES.

AIM: The association between composite dietary antioxidant index (CDAI) and hypertension remains unknown. Our study was to investigate the association of CDAI with hypertension in general adults. METHODS: A total of 21 526 participants were enrolled from the National Health and Nutrition Examination Surveys (NHANES). The CDAI was calculated from the intake of six dietary antioxidants. Multivariable logistic regressions were performed to explore the associations between CDAI and the prevalence of hypertension. Non-linear correlations were explored using restricted cubic splines. And the inflection point was determined by the two-piecewise linear regression. RESULTS: In the multivariate logistic regression model with full adjustment for confounding variables, the odds ratio (95% confidence interval) of CDAI associating with hypertension was 0.98 (0.97-1.00; P = .016). Besides, compared to the lowest quartile, the highest quartile of CDAI was associated with a lower risk of hypertension (0.81 [0.70-0.94]; P = .006). Furthermore, a linear association was found by restricted cubic spline, with 3.4 being the turning point. CONCLUSION: Our study highlighted a negative linear association between CDAI and hypertension in general adults.

Association of low-density lipoprotein-cholesterol with all-cause and cause-specific mortality.

AIMS: To explore the association between low-density lipoprotein-cholesterol (LDL-C) and all-cause and cause-specific mortality based on a prospective cohort study. METHODS: Among 10850 individuals enrolled from National Health and Nutrition Examination Survey (NHANES) 1999-2014, 1355 (12.5%) died after an average follow-up of 5.7 years. Cox proportional regression models were used to determine the association between LDL-C with the risk of mortality. RESULTS: The level of LDL-C was L-shaped associated with the risk of all-cause mortality, namely a low level was related to an increased mortality risk. The level of LDL-C associated with the lowest risk of all-cause mortality was 124 mg/dL (3.2 mmol/L) in the overall population, and 134 mg/dL (3.4 mmol/L) in individuals not receiving lipid lowering treatment. Compared with participants with LDL-C of 110-134 mg/dL (2.8-3.5 mmol/L), the multivariable adjusted hazard ratio was 1.18 (95% confidence interval 1.01 to 1.38) for individuals with the lowest quartile for all-cause mortality. In participants with coronary heart diseases, the conclusion was similar but the critical point was lower. CONCLUSIONS: We found that low levels of LDL-C increased the risk of all-cause mortality, and the lowest risk of all-cause mortality for LDL-C concentration was 124 mg/dL (3.2 mmol/L). Our results provide a reasonable range of LDL-C when to initiate a statin therapy in clinical practice.

Empagliflozin ameliorates atherosclerosis via regulating the intestinal flora.

BACKGROUND AND AIMS: Sodium-glucose cotransporter 2 inhibitor (SGLT2i) has been reported to attenuate atherosclerosis. Further, it has been suggested that intestinal flora influences atherosclerosis progression. Herein we aimed to investigate whether SGLT2i can alleviate atherosclerosis through intestinal flora. METHODS: Six-week-old male ApoE-/- mice fed a high-fat diet were gavaged either empagliflozin (SGLT2i group, n = 9) or saline (Ctrl group, n = 6) for 12 weeks. Feces were collected from both groups at the end of the experiment for fecal microbiota transplantation (FMT). Another 12 six-week-old male ApoE-/- mice were fed a high-fat diet and received FMT with feces either from SGLT2i (FMT-SGLT2i group, n = 6) or from Ctrl (FMT-Ctrl group, n = 6) groups. Blood, tissue, and fecal samples were collected for subsequent analyses. RESULTS: In comparison with Ctrl group, atherosclerosis was less severe in the SGLT2i group (p < 0.0001), and the richness of probiotic, such as f_Coriobacteriaceae, f_S24-7, f_Lachnospiraceae, and f_Adlercreutzia, was higher in feces. Besides, empagliflozin resulted in a significant reduction in the inflammatory response and altered intestinal flora metabolism. Interestingly, compared with FMT-Ctrl, FMT-SGLT2i also showed a reduction in atherosclerosis and systemic inflammatory response, as well as changes in the component of intestinal flora and pertinent metabolites similar to SGLT2i group. CONCLUSIONS: Empagliflozin seems to mitigate atherosclerosis partly by regulating intestinal microbiota, and this anti-atherosclerotic effect can be transferred through intestinal flora transplantation.

One-stage revision arthroplasty in a patient with ochronotic arthropathy accompanied by joint infection: A case report.

BACKGROUND: Ochronotic arthropathy (OcA) is a rare disease, which is caused by the accumulation of homogentisic acid in the joint. Patients with OcA have obvious joint pain and the disease progresses rapidly, eventually resulting in disability. Arthroplasty is an efficacious treatment in patients with OcA. However, when OcA patients have joint infection, is joint replacement an option? In the present report, we performed total knee arthroplasty in a patient with OcA and knee infection under the guidance of one-stage revision theory. CASE SUMMARY: A 64-year-old male was referred to our hospital due to severe left knee pain with limited mobility for 2 years. On physical examination, the patient was found to have dark brown pigmentation of the sclera and auricle. Laboratory test results showed elevations in C-reactive protein level (65.79 mg/L) and erythrocyte sedimentation rate (90.00 mm/h). The patient underwent debridement of the left knee joint, during which the cartilage surface of the knee joint was found to be black-brown in color. Bacterial culture of synovial fluid revealed Achromobacter xylosoxidans. We then carried out arthroplasty under the guidance of the theory of one-stage revision. After surgery, the patient's left knee joint pain disappeared and function recovered without joint infection. CONCLUSION: OcA accompanied by joint infection is rare. One-stage revision arthroplasty may be a treatment option for this disease.

The impact of Sacubitril/Valsartan on cardiac fibrosis early after myocardial infarction in hypertensive rats.

BACKGROUND: Sacubitril/Valsartan, a dual inhibitor of the neprilysin and angiotensin receptor, exerts cardioprotective effects in heart failure. Little is known on the impact of Sacubitril/Valsartan in hypertensive patients early post myocardial infarction. METHODS: Spontaneously hypertensive rats (SHR) were pretreated by daily angiotensin receptor blocker (ARB; 30 mg/kg intraperitoneally), Sacubitril/Valsartan (ARNI; 60 mg/kg intraperitoneally) or the same dosage of physiological saline for 1 week. Then each group underwent myocardial infarction induction and received the same treatment for another week. The blood pressure and cardiac function were evaluated prior to sacrifice. We performed histological and molecular evaluation of fibrosis in vivo and in vitro. RESULTS: The blood pressure was comparable between three groups both 1 week prior to and post myocardial infarction. ARNI and ARB restore the decreased ejection fraction (57.3 ±â€Š7.6 vs. 42.9 ±â€Š5.2%, P < 0.05; 54.3 ±â€Š6.9 vs. 42.9 ±â€Š5.2%, P < 0.01, respectively) and fractional shortening (31.6 ±â€Š5.4 vs. 22.1 ±â€Š3.1%, P < 0.05; 29.4 ±â€Š4.5 vs. 22.1 ±â€Š3.1%, P < 0.05, respectively) post myocardial infarction. The infarct size and collagen deposition were also significantly mitigated in ARNI and ARB groups. In addition, ARNI and ARB treatment reduced the expression of cardiac remodeling-related factors, such as Bnp, α-SMA, Vimentin, and Col1a1 (all P < 0.05 vs. MI group). Finally, ARNI and ARB decreased the expression of α-SMA in cardiac fibroblasts treated with Ang II. CONCLUSION: In conclusion, pretreatment with ARNI maintained cardiac function and reduced myocardial fibrosis in myocardial infarction, probably prior to any anti-hypertensive effect.

M2-like macrophages transplantation protects against the doxorubicin-induced heart failure via mitochondrial transfer.

AIMS: The alternatively activated macrophages have shown a cardioprotective effect in heart failure. However, the effect of M2 adoptive transfer in non-ischemic heart failure is unknown. In this study, we evaluated the efficacy of M-CSF plus IL-4 induced M2-like macrophages transplantation in doxorubicin-induced cardiotoxicity. METHODS: Bone marrow mononuclear cells were polarized as CCR2+CD206+ M2-like macrophages by a combination of M-CSF plus IL-4 treatment. C57BL/6 mice received a single intraperitoneal injection of doxorubicin (15 mg/kg). The treatment group were treated with M2-like macrophages (1 × 10^6 cells per mouse; i.v.) once a week for 2 weeks. After 3 weeks, we examined the percentage of resident cells and cardiac function. Furthermore, we evaluated cardiac fibrosis, cardiomyocyte apoptosis and circulating inflammatory factors. Finally, we investigated the mitochondria transfer in vitro in a direct and indirect co-culture conditions. RESULTS: Cardiac function was significantly improved in doxorubicin-induced heart failure by adoptive transfer of M2-like macrophages. Besides, M2-like macrophages treatment attenuated cardiac fibrosis and cardiomyocyte apoptosis, as well as increased the level of circulating IL-4 and Th2 response. In vitro, M2-like macrophages could transfer mitochondria to injured cardiomyocytes in a direct and indirect way. CONCLUSIONS: In our study, adoptive transfer of M2-like macrophages could protect against the doxorubicin-induced cardiotoxicity, which may be partly attributed to mitochondria transfer. And M2-like macrophages transplantation could become a treatment for non-ischemic heart failure in the clinical practice.

Percutaneous intravenous catheter forceps biopsy in right atrial mass: two case reports and literature review.

BACKGROUND: Primary malignant tumors of the heart are rare. Although preoperative histological diagnosis is difficult, it has paramount value in therapeutic strategy development and prognostic estimation. Herein, we reported 2 cases of intracardiac tumors. CASES PRESENTATION: Both patients presented to the hospital with heart-related symptoms. Echocardiography showed massive masses in the atrium and positron emission tomography-computed tomography (PET/CT) revealed hypermetabolism and invasiveness. One patient cannot take surgery due to extensive metastasis and poor condition. The other patient was primarily diagnosed with lymphoma, and surgery was not recommended. They successfully underwent intravenous atrial biopsy, and histological samples confirmed intimal sarcoma and diffuse large B cell lymphoma. Based on immunohistochemical and molecular assessments, targeted chemotherapy was administered, resulting in clinical and imaging remission at discharge. CONCLUSIONS: Percutaneous intravenous catheter biopsy as a safe invasive test provides an accurate pathological diagnosis after imaging evaluation, and offers a therapeutic direction. Nonmalignant masses and some chemo-radiosensitive malignant tumors in the atrium could have good prognosis after targeted therapy.

Triglyceride Glucose Index Was Associated With the Risk of Peripheral Artery Disease.

This study aims to investigate the relationship between the triglyceride glucose (TyG) index and peripheral artery disease (PAD). A total of 3125 participants with completed TyG and ankle brachial pressure index (ABPI) records were enrolled from the National Health and Nutrition Examination Survey (NHANES) cycle of 1999-2004. The TyG index was calculated as ln [triglycerides (mg/dL) × glucose (mg/dL)/2], and the presence of PAD was defined as ABPI ≤.9. The participants were 59.9 ± 12.9 years old and 51.5% (1608) were male. The prevalence of PAD was 7.2% (225). Compared with the reference lowest quartile of TyG index, the highest quartile was associated with 1.27-fold increased (odds ratio [OR] 2.27, 95% confidence interval [CI] 1.53-3.41; P < .001) risk of PAD. After adjusting for sociodemographic, lifestyles, and cardiometabolic factors, the multivariate-adjusted OR and 95% CI were 1.74 (1.02-3.01; P = .044) in participants within the highest quartile. Subgroup analysis showed that the association between TyG index and the risk of PAD was still consistent across subgroups. In conclusion, higher TyG index was significantly associated with the higher risk of PAD, which could be a marker of PAD.

Association between the urinary nickel and the diastolic blood pressure in general population.

AIM: To investigate the association of the level of nickel and blood pressure (BP) level in a general population. METHODS: A total of 2201 participants were enrolled from the National Health and Nutrition Examination Surveys (NHANES) 2017-2018. Urinary nickel level was measured using inductively coupled-plasma mass spectrometry. Multivariable linear regressions were performed to explore the associations between nickel and systolic BP and diastolic BP. Restricted cubic splines were used to explore the nonlinearity. RESULTS: Per one-fold increase of nickel was associated with a 0.67-unit decrease of diastolic BP (ß -0.67, 95 % confidence interval [CI] [-1.15, -0.18]; p = 0.007). Comparing with the lowest quartile, the highest quartile decreased 2.21-unit diastolic BP (ß -2.21, 95 % CI [-3.84, -0.59]; p = 0.007). Restricted cubic spline confirmed the relationship was linear. Subgroup analysis found that the association was only significant in population without hypertension. CONCLUSIONS: The urinary nickel, as a long-term exposure biomarker, was associated with the diastolic BP in individuals without hypertension.

Association between hemoglobin glycation index and subclinical myocardial injury in the general population free from cardiovascular disease.

BACKGROUND AND AIMS: The relationship between hemoglobin glycation index (HGI) and the diagnosis and prognosis of cardiovascular disease (CVD) has been verified by previous studies. However, it remains unknown whether HGI has a predictive effect on subclinical myocardial injury (SC-MI). The purpose of the present study was to explore the relationship between HGI and SC-MI in the general population free from CVD. METHODS AND RESULTS: The present study included 6009 participants free of CVD from the third National Health and Nutrition Examination Survey. Binary Logistic regression analysis was used to tested the association between HGI and SC-MI. As results, the HGI was significantly higher in participants with SC-MI compared with those without, and the HGI was positively correlated with SC-MI and other metabolic disorder parameters. Each 1-unit increase of HGI and glycated hemoglobin A1c (HbA1c) was independently associated with higher risk of SC-MI (P < 0.05), while fasting plasma glucose (FPG) was no longer a predictive indicator of SC-MI with the increase of confounding factors [OR (95% CI): 1.001 (0.999-1.003), P = 0.305]. And in the subgroup analysis, HGI, only in participants without diabetes, was independently associated with higher risk of SC-MI, while HbA1c and FPG had no independent predictive role in both diabetic and non-diabetic participants. CONCLUSIONS: HGI was a significant predictor of SC-MI in the general population free from CVD.

Ultrasmall Fe(III)-Tannic Acid Nanoparticles To Prevent Progression of Atherosclerotic Plaques.

Macrophage accumulation is central to the pathogenesis of atherosclerotic plaques. Reducing macrophages in plaques is an appealing approach to attenuate the development of atherosclerosis. Chemodynamic therapy, specifically inhibiting hydrogen peroxide (H2O2)-rich cells in slightly acidic microenvironment, has emerged as a new method in tumor treatment. Herein, we manufactured ultrasmall dopamine-modified hyaluronic acid (HD)-stabilized Fe(III)-tannic acid nanoparticles (HFTNPs). HFTNPs can specifically accumulate in inflammatory macrophages in atherosclerotic plaques, provide brighter magnetic resonance images, promote reactive oxygen species (ROS) generation, and induce the death of inflammatory macrophages without damaging normal cells and tissues. In conclusion, HFTNPs have a tremendous potential as safe and effective diagnostic and therapeutic reagents for atherosclerosis.

Empagliflozin Alleviates Atherosclerosis Progression by Inhibiting Inflammation and Sympathetic Activity in a Normoglycemic Mouse Model.

BACKGROUND: Recent clinical studies have revealed that sodium glucose co-transporter 2 inhibitors (SGLT2i) reduced cardiovascular events in type 2 diabetes. Here, we investigated whether empagliflozin, as a kind of SGLT2i, could alleviate atherosclerosis progression in non-diabetic mice. METHODS: ApoE-/- mice were fed on a western diet for 12 weeks to induce atherosclerosis. The treatment group of mice was treated with drinking water containing empagliflozin (10mg/kg/day). On the 12th week, the whole aortas of each group were harvested. HE and Movat staining were performed for atherosclerotic lesion area and size. CD 68 and MCP-1 immunohistochemistry were used to evaluate inflammatory cell infiltration. Mouse serum lipid profiles (total cholesterol, triglyceride, low-density lipoprotein-C, and high-density lipoprotein-C), systemic inflammation level (IL-1ß, IL-6 and IL-10), renin-angiotensin-aldosterone system (RAAS) and sympathetic activity (norepinephrine and neuropeptide Y) were measured by ELISA. RESULTS: Empagliflozin could reduce the atherosclerotic lesion areas. Specifically, empagliflozin could significantly decreased inflammatory levels, RAAS and sympathetic activity in vivo. In vitro studies also showed that empagliflozin could inhibit IL-1ß expression in oxLDL-treated macrophages by regulating NF-κB signaling. CONCLUSION: Empagliflozin could prevent atherosclerosis by repressing inflammation and sympathetic activity.

PM2.5 induces endothelial dysfunction via activating NLRP3 inflammasome.

PM2.5 (particulate matter <2.5 µm in diameter) is proven to contribute to the development of atherosclerosis. Endothelial cell dysfunction is the initial step of atherosclerosis. The underlying mechanisms of endothelial cell damage exposed to PM2.5 are still obscure. In our study, PM2.5 was administrated to C57BL/6 male mice by intranasal instillation for 2 weeks. Human umbilical vein endothelial cells (HUVECs) were also treated with PM2.5 to evaluate the adverse effect in vitro. The immunohistochemical staining of aortas showed that the expressions of proinflammatory cytokines and endothelial adhesion markers were significantly increased in PM2.5-exposed mice than that in saline-exposed mice. In vitro, PM2.5 could inhibit HUVECs viability and impair cell migration in a concentration-dependent manner. Besides, PM2.5 exposure downregulated eNOS expression while upregulated reactive oxygen species (ROS) levels. Mechanistically, PM2.5 activated the NLRP3 inflammasome in HUVECs while knockdown of NLRP3 could effectively reverse the downregulation of eNOS expression and production of ROS after PM2.5 exposure. In summary, our data showed that PM2.5 could cause endothelial dysfunction, and probably via NLRP3 inflammasome activation.

Osteoporosis was associated with severe abdominal aortic calcification based on a cross-sectional study.

Abdominal aortic calcification and osteoporosis are age-related diseases. Based on a nationally representative US population, we concluded that osteoporosis may be independently associated with severe abdominal aortic calcification, which could improve our insights into the prevention and management of vascular disease. INTRODUCTION: Abdominal aortic calcification (AAC) and osteoporosis are age-related diseases and share similar pathological mechanisms. However, the association between osteoporosis and AAC is uncertain. METHODS: A total of 3134 participants with complete record of AAC score calculated from dual-energy X-ray absorptiometry (DXA) were enrolled from the National Health and Nutrition Examination Survey (NHANES) 2013-2014. The diagnosis of osteoporosis was obtained from self-reported interview. The baseline covariates were compared between participants with and without osteoporosis. Multivariable logistic regression was performed to examine the association between abdominal aortic calcification and osteoporosis. RESULTS: Compared with those without osteoporosis, participants with osteoporosis had higher AAC scores. Osteoporosis was positively associated with higher odds of severe AAC (OR = 2.65; 95%CI, 1.89-3.71; P < 0.001), and the association was not altered (OR = 2.17; 95%CI, 1.23-3.83; P = 0.008) after adjusting for numerous covariates. CONCLUSIONS: Our findings suggest that osteoporosis may be independently associated with severe abdominal aortic calcification.