대한신장학회

논문분류	춘계학술대회 초록집
제목	Renal Fibrosis: Understanding the Function and Mechanisms of TMEM52B
저자	Rui Xue
출판정보	2024; 2024(1):
키워드
초록	Objectives: Renal tubulointerstitial fibrosis stands out as the primary pathological hallmark contributing to kidney impairment and represents a fundamental progression toward end-stage renal disease. Our investigation, utilizing exome sequencing across various human organs and tissues, has revealed a notable enrichment of transmembrane protein 52B (TMEM52B) expression within the kidney, highlighting its close association with renal function. Consequently, our forthcoming research endeavors aim to delve deeper into elucidating the precise role and underlying mechanisms of TMEM52B specifically in tubular injury, with a particular focus on renal tubulointerstitial fibrosis. Methods: We employed CRISPR-Cas9 technology to construct TMEM52B gene system knockout C57BL/6 mice. Subsequently, we performed unilateral ureteral obstruction (UUO) surgery to induce renal injury and tubulointerstitial fibrosis. Following the surgery, we then conducted a series of analyses and proteomics testing to investigate the changes after TMEM52B knockout. Finally, we conducted additional in vitro experiments to further validate the molecular mechanism of TMEM52B in renal fibrosis. Results: Firstly, qPCR results showed that TMEM52B expression in TMEM52B knockout mice was nearly absent. TMEM52B system knockout mice exhibited even more severe renal tubular injury in the UUO model. Additionally, immunohistochemistry and qPCR results revealed a significant increase in fibrosis marker expression in TMEM52B system knockout mice in the UUO model. Proteomic analysis showed Myeloid-Derived Growth Factor (MYDGF) expression was significantly decreased in the kidney tissue of UUO model mice, and further markedly decreased in TMEM52B system knockout UUO model mice. In vitro, TMEM52B expression significantly decreased under TGF-β1 stimulation, and altering TMEM52B levels correspondingly changed MYDGF expression. Conclusions: The diminishment of TMEM52B is poised to escalate renal tubular injury and exacerbate tubulointerstitial fibrosis, a cascade potentially orchestrated through the modulation of MYDGF. Targeting TMEM52B could be a novel and potential therapeutic strategy to alleviate renal tubular injury and interstitial fibrosis, thus delaying the progression of kidney disease.
원문(PDF)	PDF 원문보기

간행물 검색

대한신장학회 회원관리 규정