주권욱 교수
Kwon Wook Joo
서울대학교 · 의학
연구실 소개
주권욱 교수의 연구실은 만성 신장질환의 발달 기전과 치료 전략을 중심으로 신장 세포의 손상, 산화 스트레스, 염증 반응, 섬유화 과정에 대한 분자 기전을 규명하고 있습니다. 특히 리튬 유도성 신성다뇨증, IgA 신염의 유전적 소인, DPP4 억제제 및 HIF 활성화제 등의 신약 작용 기전을 탐색하며, 신장 기능 보존과 만성 신장질환 예방을 위한 기초 및 번역 연구를 수행하고 있습니다. 또한 수면 부족이 만성 신장질환 위험에 미치는 영향 등 생활습관과 신장 건강의 상관관계에 대해서도 관심을 기울이고 있습니다.
연구 현황
연구 성과 추이
표시된 성과는 수집된 데이터 기준으로 산출되며, 일부 차이가 있을 수 있습니다.
주요 논문
15Thiazides have been used in patients with nephrogenic diabetes insipidus (NDI) to decrease urine volume, but the mechanism by which it produces the paradoxic antidiuretic effect remains unclear. Previous studies have reported that downregulation of aquaporin-2 (AQP2) is important for the development of lithium-induced (Li-induced) polyuria and that hydrochlorothiazide (HCTZ) increases renal papillary osmolality and Na(+) concentration in Brattleboro rats. For elucidating the molecular basis of t
In this study, the incidence of allopurinol-induced SCARs was considerably high in CRI patients with HLA-B58. This finding indicates that the presence of HLA-B58 may increase the risk of allopurinol-induced SCARs. Screening tests for HLA-B58 in CRI patients will be clinically helpful in preventing severe allopurinol hypersensitivity reactions.
Activation of HIF by DMOG halted the progression of proteinuria and attenuated structural damage by preventing podocyte injury in the remnant kidney model. This renoprotection was accompanied by a reduction of oxidative stress, inflammation and fibrosis.
Machine learning algorithms increase the accuracy of mortality prediction for patients undergoing CRRT for acute kidney injury compared with previous scoring models.
In patients with CKD, dapagliflozin prolonged survival irrespective of baseline patient characteristics. The benefits were driven largely by reductions in non-cardiovascular death.
Clinicians may consider implementing the SPARK index and classifications to stratify patients' PO-AKI risks before performing noncardiac surgery.
Korea Healthcare Technology R&D Project, Ministry of Health and Welfare, Republic of Korea.
In rat remnant kidneys, DPP IV inhibitor attenuated renal dysfunction and structural damage. A reduction of apoptosis, inflammation and an increase of antioxidant could be suggested as a renoprotective mechanism together with the activation of FoxO3a signaling. Therefore, DPP IV inhibitors might provide a promising approach for treating CKD, but their application in clinical practice remains to be investigated.
TNF superfamily member 13 (TNFSF13) has been identified as a susceptibility gene for IgA nephropathy in recent genetic studies. However, the role of TNFSF13 in the progression of IgA nephropathy remains unresolved. We evaluated two genetic polymorphisms (rs11552708 and rs3803800) and plasma levels of TNFSF13 in 637 patients with IgA nephropathy, and determined the risk of ESRD according to theses variable. Neither of the examined genetic polymorphisms associated with a clinical outcome of IgA ne
Proton-secretory defect is thought to be a major pathophysiologic mechanism leading to classic distal renal tubular acidosis (dRTA). However, there have been only two case reports demonstrating the absence of proton pump in renal tissues of the patients with Sjögren's syndrome. This study presents two cases of classic dRTA in which the absence of intact H(+)-ATPase was shown in their renal biopsy tissues by immunohistochemistry using a rabbit polyclonal antibody against the 70 kDa catalytic subu
In this study, the effect of glycemic control differed according to age and dialysis type in diabetic patients. Thus, the target of glycemic control should be customized; further observational studies may strengthen the clinical relevance.
A screening program should be necessary for urinary tract cancer in Korean patients with ESRD. Cancer screening programs for patients with ESRD in Korea should be emphasized on female patients and patients with non-diabetic ESRD.
Macrophage infiltration has been observed in the renal biopsy specimens of diabetic nephropathy (DN), and hyperglycemic state stimulates the renal expression of RANTES (regulated upon activation, normal T-cell expressed and secreted) and MCP- 1 (monocyte chemoattractant protein-1). Upregulation of RANTES and MCP-1 with infiltrating macrophages may play a crucial role in the development and progression of DN. Genetic polymorphisms of RANTES and its receptors were reported to be independent risk f
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