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Aim/introduction: Senescence is a key driver of age-related kidney dysfunction, including diabetic kidney disease. Oxidative stress activates cellular senescence, induces abnormal glycolysis, and is associated with pyruvate kinase muscle isoform 2 (PKM2) dysfunction; however, the mechanisms linking PK activation to cellular senescence have not been elucidated. We hypothesized that PKM2 activation by TEPP-46 could suppress oxidative stress-induced renal tubular cell injury and cellular senescence.

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Objective: The effectiveness of using as an adjuvant therapy for patients with renal dysfunction (RD), especially acute kidney injury (AKI), is still a topic of debate. In response to the current conflicting data, the present meta-analysis was conducted to assess the clinical effectiveness of in the treatment of RD and to provide evidence for clinical practice.

Methods: Several databases, including PubMed, EMBASE, Cochrane Library, China National Knowledge Infrastructure (CNKI) and Wanfang, were systematically searched updated to March 25, 2024.

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Background And Objective: Mitochondria are crucial to the function of renal tubular cells, and their dynamic perturbation in many aspects is an important mechanism of diabetic kidney disease (DKD). Single-nucleus RNA sequencing (snRNA-seq) technology is a high-throughput sequencing analysis technique for RNA at the level of a single cell nucleus. Here, our DKD mouse kidney single-cell RNA sequencing conveys a more comprehensive mitochondrial profile, which helps us further understand the therapeutic response of this unique organelle family to drugs.

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A novel, dominant disease mechanism of distal renal tubular acidosis with specific variants in ATP6V1B1.

Nephrol Dial Transplant

January 2025

Paediatric Nephrology, UZ Leuven and Department of Cellular and Molecular Physiology, KUL, Leuven, Belgium.

Background And Hypothesis: ATP6V1B1 encodes a subunit of the vacuolar H+-ATPase and pathogenic variants are associated with autosomal recessive distal renal tubular acidosis (dRTA) with deafness. Heterozygous variants predicted to affect a specific amino acid, Arg394, have been recurrently reported in dRTA but their significance has been unclear. We hypothesised that these variants are associated with a dominant disease mechanism.

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Methyltransferase-like 3 mediates m6A modification of heme oxygenase 1 mRNA to induce ferroptosis of renal tubular epithelial cells in acute kidney injury.

Free Radic Biol Med

January 2025

Traditional Chinese Medicine Integrated Department of Nephrology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan Province, China; Research Institute of Nephrology, Zhengzhou University, Zhengzhou, Henan province, China; Henan Province Research Center for Kidney Disease, Zhengzhou, Henan Province, China; Key Laboratory of Precision Diagnosis and Treatment for Chronic Kidney Disease in Henan Province, Zhengzhou, Henan Province, China; Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, Henan Province, China; Innovation Center of Basic Research for Metabolic-Associated Fatty Liver Disease, Ministry of Education of China, Zhengzhou, Henan Province, China. Electronic address:

Acute kidney injury (AKI) involves a series of syndromes characterized by a rapid increase in creatinine levels. Ferroptosis, as an iron-dependent mode of programmed cell death, reportedly participates in the pathogenesis of AKI. Methyltransferase-like 3 (METTL3)-mediated m6A modification has been recently associated with various kidney diseases; however, the mechanism of METTL3 crosstalk with the molecules involved in ferroptosis is not clearly understood.

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