문주영 교수

IL-1β-secreting nucleotide-binding oligomerization domain protein 3 (NLRP3) inflammasomes play a pivotal role in triggering innate immune responses in metabolic disease. We investigated the role of soluble uric acid in NLRP3 inflammasome activation in macrophages to demonstrate the effect of systemic hyperuricemia on progressive kidney damage in type 2 diabetes. THP-1 cells, human acute monocytic leukemia cells, were cultured to obtain macrophages, and HK-2 cells, human renal proximal tubule cel

Asymptomatic hyperuricemia is frequently observed in patients with kidney disease. Although a substantial number of epidemiologic studies have suggested that an elevated uric acid level plays a causative role in the development and progression of kidney disease, whether hyperuricemia is simply a result of decreased renal excretion of uric acid or is a contributor to kidney disease remains a matter of debate. Over the last two decades, multiple experimental studies have expanded the knowledge of

BACKGROUND/AIMS: Recent evidence has shown that an inflammatory process is involved in the development and progression of diabetic nephropathy. This study examined the impact of activated intrarenal lymphocytes in this inflammatory process. METHODS: We studied T cell recruitment in mice with streptozotocin (STZ)-induced diabetes by flow cytometry and immunohistochemistry. The kidney biopsy specimens from patients with type 2 diabetes mellitus and diabetic nephropathy were evaluated by immunohist

Cytoplasmic nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) forms an inflammasome with apoptosis-associated speck-like protein containing a CARD (ASC) and pro-caspase-1, which is followed by the cleavage of pro-caspase-1 to active caspase-1 and ultimately the activation of IL-1β and IL-18 and induction of pyroptosis in immune cells. NLRP3 activation in kidney diseases aggravates inflammation and subsequent fibrosis, and this effect is abrogated by genetic or pharmacolog

The NOD-like receptor family, pyrin domain containing-3 (NLRP3) inflammasome has been implicated in renal inflammation and fibrosis. However, the biological function of inflammasome-independent NLRP3 in non-immune cells is still unclear. We evaluated the role of inflammasome-independent NLRP3 in renal tubular cells and assessed the value of NLRP3 as a therapeutic target for acute kidney injury (AKI). Various renal tubular cell lines and primary cultured tubular cells from NLRP3 knockout (KO) mic

Angiotensin II (Ang II)-induced activation of nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase leads to increased production of reactive oxygen species (ROS), an important intracellular second messenger in renal disease. Recent findings suggest that Ang II induces mitochondrial depolarization and further amplifies mitochondrial generation of ROS. We examined the hypothesis that ROS injury mediated by Ang II-induced mitochondrial Nox4 plays a pivotal role in mitochondrial dysfunction

ANG-(1-7) is associated with vasodilation and nitric oxide synthase stimulation. However, the role of ANG-(1-7) in type 2 diabetes mellitus is unknown. In this study, we examined the hypothesis that ANG-(1-7) attenuates ANG II-induced reactive oxygen species stress (ROS)-mediated injury in type 2 diabetic nephropathy of KK-A(y)/Ta mice. KK-A(y)/Ta mice were divided into four groups: 1) a control group; 2) ANG II infusion group; 3) ANG II+ANG-(1-7) coinfusion group; and 4) ANG II+ANG-(1-7)+d-Ala(

The activation of renin-angiotensin-aldosterine system(RAAS) is one of the main pathogenesis of hypertension. All the components of RAAS are present in the kidneys at higher concentrations compared to plasma levels, and intrarenal formation of angiotensin II (Ang II) is independent of the systemic RAAS. There are some unique features in intrarenal RAAS compared to systemic RAAS. Unlike JG cells where Ang II inhibits renin release via the AngII type 1 (AT1) receptor by negative feedback, in the c

OBJECTIVE: Despite percutaneous fluoroscopy ensuring appropriate placement of peritoneal dialysis (PD) catheters, the efficacy of this method is not well known. Therefore, we evaluated our long-term experience with fluoroscopy-assisted placement of PD catheters. PATIENTS AND METHODS: We retrospectively reviewed 134 PD catheters in 114 PD patients that were treated in the PD center of a university-based hospital. We evaluated complications related to PD catheters, causes for catheter removal, and

Monocyte chemoattractant protein-1 (MCP-1) is suggested to be involved in the progression of diabetic nephropathy. We investigated the association of the -2518 A/G polymorphism in the MCP-1 gene with progressive kidney failure in Korean patients with type 2 diabetes mellitus (DM). We investigated -2518 A/G polymorphism of the MCP-1 gene in type 2 DM patients with progressive kidney failure (n=112) compared with matched type 2 DM patients without nephropathy (diabetic control, n=112) and healthy

Gemigliptin exerted non-glucoregulatory protective effects on both diabetic nephropathy and cardiomyopathy. However, high-level inhibition of DPP-4 was associated with an organ-specific effect on cardiovascular complications in type 2 diabetes.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a promising new target for the prevention of cardiovascular (CV) events. However, the clinical significance of circulating PCSK9 is unclear in hemodialysis (HD) patients. A total of 353 HD patients were prospectively enrolled from June 2016 to August 2019 in a K-cohort. Plasma PCSK9 level was measured at the time of study enrollment. The primary endpoint was defined as a composite of CV event and death. Plasma PCSK9 level was positively co

BACKGROUND/AIM: The role of angiotensin-converting enzyme (ACE)-related carboxypeptidase-2 (ACE2) in the regulation of the renin-angiotensin system is not well characterized. This study investigated the changes in the expression of ACE and ACE2 in the kidney in early diabetic rats. METHODS: Streptozotocin-induced diabetic rats were examined. The concentrations of angiotensin II in plasma, urine, and renal cortex were measured by radioimmunoassay. The mRNA expression of ACE, ACE2, angiotensin II

목 적 : 최근 한국에서 산모 연령 변화와 고령산모가 증가하는 경향을 파악하고 그 비율을 살펴보고, 고령산모의 증가가 저체중출생의 원인이 되는지 알아보고자 하였다. 방 법 : 1995, 2000, 2005, 2008년 한국통계포털(통계청)에서 공개한 한국의 출생통계 자료를 이용하였다. 조사대상은 각 연도별 한국의 총 출생아 수이며, 출생 시 그들 산모의 나이 분포는 15세 미만부터 50세 이상까지 가임기 여성 전체를 대상으로 하였고, 각 연도별 출생아 수는 각각 71만5천, 63만4천, 43만5천, 46만5천명이었다. 출생아의 분포를 출생 체중을 기준으로 구분하였으며, 각 연도별 산모 연령 분포와 35세 이상의 고령 산모의 비율을 조사하고, 고령 산모에서 저체중출생아의 출생 빈도를 후향적으로 분석하였다. 결 과 : 조사기간 동안 출생아 수는 지속적으로 감소하였으나, 저출생체중아의 빈도는 증가하였다. 산모의 연령 분포는 1995, 2000, 2005, 2008년 연도별로, 25-29세