O‐linked β‐N‐acetylglucosamine (O‐GlcNAc) modification: Emerging pathogenesis and a therapeutic target of diabetic nephropathy DOI Creative Commons

Bingxue Qi,

Yang Chen,

Siyang Chai

и другие.

Diabetic Medicine, Год журнала: 2024, Номер unknown

Опубликована: Сен. 16, 2024

Abstract Aims O‐Linked β‐N‐acetylglucosamine (O‐GlcNAc) modification, a unique post‐translational modification of proteins, is elevated in diabetic nephropathy. This review aims to summarize the current knowledge on mechanisms by which O‐GlcNAcylation proteins contributes pathogenesis and progression nephropathy, as well therapeutic potential targeting O‐GlcNAc for its treatment. Methods Current evidence literature was reviewed synthesized narrative review. Results Hyperglycemia increases glucose flux into hexosamine biosynthesis pathway, activates glucosamino‐fructose aminotransferase expression activity, leading production substrate UDP‐GlcNAc an increase protein kidney cells. Protein regulates function cells including mesangial cells, podocytes, proximal tubular promotes renal interstitial fibrosis, resulting damage. treatments such sodium‐glucose cotransporter 2 (SGLT‐2) inhibitors renin–angiotensin–aldosterone system (RAAS) inhibitors, delay disease progression, suppress O‐GlcNAcylation. Conclusions Increased mediates cell damage Although full significance inhibition not yet understood, it may represent novel target treating

Язык: Английский

Single-cell atlas reveals multi-faced responses of losartan on tubular mitochondria in diabetic kidney disease DOI Creative Commons
Zhen Zhu, Guangxin Luan, Song Wu

и другие.

Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)

Опубликована: Янв. 21, 2025

Mitochondria are crucial to the function of renal tubular cells, and their dynamic perturbation in many aspects is an important mechanism diabetic kidney disease (DKD). Single-nucleus RNA sequencing (snRNA-seq) technology a high-throughput analysis technique for at level single cell nucleus. Here, our DKD mouse single-cell conveys more comprehensive mitochondrial profile, which helps us further understand therapeutic response this unique organelle family drugs. After high fat diet (HFD), mice were intraperitoneally injected with streptozotocin (STZ) induce DKD, then divided into three subsets: CON (healthy) subset, (vehicle) LST (losartan; 25 mg/kg/day) subset. Divide HK-2 LG (low glucose; 5 mM) HG (high 30 + 1 µ M) subsets. snRNA-seq was performed on tissues subset mice. To reveal effects losartan gene pathway changes mitochondria, Gene Ontology (GO) enrichment GSEA/GSVA scoring analyze specific proximal (PT) mitochondria treatment, including key events homeostasis such as morphology, dynamics, mitophagy, autophagic flux, respiratory chain, apoptosis, ROS generation. Preliminary validation through vitro vivo experiments, observation morphology dynamics using probes Mitotracker Red, evaluation effect electron microscopy, laser confocal immunofluorescence, Western blotting. Detection flux cells by transfecting Ad-mCherry-GFP-LC3B dual fluorescence labeled adenovirus. Various fluorescent energy detector used detect ROS, respiration mitochondrion. Through atlas kidneys, it found that treatment significantly increased percentage PT cells. differentially expressed genes showed autophagy mitochondrion pathway. Further GSEA GSVA revealed mitophagy other events, production, membrane potential, adenosine triphosphate (ATP) synthesis, involved protective thereby improving homeostasis. Consistent results also obtained cellular experiments. In addition, we highlighted subpopulation phenotype data, preliminarily validated co-localization expression Pink1 Gclc specimens patients treated losartan. Our research suggests scRNA-seq can reflect multifaceted landscape after drug these findings may provide new targets therapy level.

Язык: Английский

Процитировано

1

Tangshenning Formula Alleviates Tubular Injury in Diabetic Kidney Disease via the Sestrin2/AMPK/PGC-1α Axis: Restoration of Mitochondrial Function and Inhibition of Ferroptosis DOI
Xiaomeng Shan,

Cong Lu,

Chun‐Wei Chen

и другие.

Journal of Ethnopharmacology, Год журнала: 2025, Номер 345, С. 119579 - 119579

Опубликована: Март 3, 2025

Язык: Английский

Процитировано

0

O‐linked β‐N‐acetylglucosamine (O‐GlcNAc) modification: Emerging pathogenesis and a therapeutic target of diabetic nephropathy DOI Creative Commons

Bingxue Qi,

Yang Chen,

Siyang Chai

и другие.

Diabetic Medicine, Год журнала: 2024, Номер unknown

Опубликована: Сен. 16, 2024

Abstract Aims O‐Linked β‐N‐acetylglucosamine (O‐GlcNAc) modification, a unique post‐translational modification of proteins, is elevated in diabetic nephropathy. This review aims to summarize the current knowledge on mechanisms by which O‐GlcNAcylation proteins contributes pathogenesis and progression nephropathy, as well therapeutic potential targeting O‐GlcNAc for its treatment. Methods Current evidence literature was reviewed synthesized narrative review. Results Hyperglycemia increases glucose flux into hexosamine biosynthesis pathway, activates glucosamino‐fructose aminotransferase expression activity, leading production substrate UDP‐GlcNAc an increase protein kidney cells. Protein regulates function cells including mesangial cells, podocytes, proximal tubular promotes renal interstitial fibrosis, resulting damage. treatments such sodium‐glucose cotransporter 2 (SGLT‐2) inhibitors renin–angiotensin–aldosterone system (RAAS) inhibitors, delay disease progression, suppress O‐GlcNAcylation. Conclusions Increased mediates cell damage Although full significance inhibition not yet understood, it may represent novel target treating

Язык: Английский

Процитировано

2