Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Objective: Diabetic nephropathy (DN), characterized by a complex and multifaceted pathogenesis, stands as the foremost catalyst behind end-stage renal disease (ESRD). This study aims to analyze the level and non-metabolic role of glomerular aldolase B (ALDOB) in DN progression.
Methods: Glomerular proteomics and transcriptome are analyzed from 50 DN patients and 25 controls, respectively. Human kidney biopsy, cultured podocytes and mouse models are employed to study ALDOB levels and function.
Results: ALDOB is strongly downregulated in DN-affected glomeruli, as well as in human and murine podocytes exposed to inflammatory cytokines. ALDOB reduction increases podocyte injury, while adenovirus-mediated ALDOB overexpression leads to substantial alleviation of renal injuries in a diabetic mouse model. Mechanistically, ALDOB reduction triggers the Akt/GSK/β-catenin signaling cascade within podocytes.
Conclusion: Our findings reveal a novel non-metabolic role of glomerular ALDOB in protecting against podocyte injury and renal fibrosis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jare.2024.12.027 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Loss of glomerular aldolase B in diabetic nephropathy promotes renal fibrosis via activating Akt/GSK/β-catenin axis.
J Adv Res
December 2024
State Key Laboratory of Pharmaceutical Biotechnology, Department of Gastroenterology, Drum Tower Hospital, Nanjing University, School of Life Sciences, Nanjing, Jiangsu 210093, China. Electronic address:
Objective: Diabetic nephropathy (DN), characterized by a complex and multifaceted pathogenesis, stands as the foremost catalyst behind end-stage renal disease (ESRD). This study aims to analyze the level and non-metabolic role of glomerular aldolase B (ALDOB) in DN progression.
Methods: Glomerular proteomics and transcriptome are analyzed from 50 DN patients and 25 controls, respectively.
HOGA1 variants in Chinese patients with primary hyperoxaluria type 3: genetic features and genotype-phenotype relationships.
World J Urol
August 2023
Department of Urology, Beijing Friendship Hospital, Capital Medical University, 95 YongAn Road, Xicheng District, Beijing, 100050, China.
Purpose: The aim of our study is to describe the genetic features and correlation between the genotype and phenotype of Chinese patients with primary hyperoxaluria type 3 (PH3).
Methods: The genetic and clinical data of PH3 patients in our cohort were collected and analyzed retrospectively. All published studies of Chinese PH3 populations between January 2010 and November 2022 were searched and enrolled based on inclusive standards.
Characterization of Stone Events in Patients With Type 3 Primary Hyperoxaluria.
J Urol
June 2023
Divison of Nephrology and Hypertension, Mayo Clinic, Rochester, Minnesota.
Purpose: Hallmarks of primary hyperoxaluria type 3 are nephrolithiasis and hyperoxaluria. However, little is known about factors influencing stone formation in this disease. We characterized stone events and examined associations with urine parameters and kidney function in a primary hyperoxaluria type 3 population.
View Article and Find Full Text PDFPFKP Activation Ameliorates Foot Process Fusion in Podocytes in Diabetic Kidney Disease.
Front Endocrinol (Lausanne)
March 2022
Division of Nephrology, Renmin Hospital of Wuhan University, Wuhan, China.
Background: Glycolysis dysfunction is an important pathogenesis of podocyte injury in diabetic kidney disease (DKD). Foot process fusion of podocytes and increased albuminuria are markers of early DKD. Moreover, cytoskeletal remodeling has been found to be involved in the foot process fusion of podocytes.
View Article and Find Full Text PDFPrimary Hyperoxaluria Type 3 Can Also Result in Kidney Failure: A Case Report.
Am J Kidney Dis
January 2022
Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN; Division of Pediatric Nephrology and Hypertension, Mayo Clinic, Rochester, MN. Electronic address:
Primary hyperoxaluria (PH) is a group of genetic disorders that result in an increased hepatic production of oxalate. PH type 3 (PH3) is the most recently identified subtype and results from mutations in the mitochondrial 4-hydroxy-2-oxoglutarate aldolase gene (HOGA1). To date, there have been 2 cases of kidney failure reported in PH3 patients.
View Article and Find Full Text PDF