Evaluation of urinary autophagy transcripts expression in diabetic kidney disease

Matboli, Marwa; Azazy, Ahmed Em; Adel, Seham; Bekhet, Miram M.; Eissa, Sanaa

doi:10.1016/j.jdiacomp.2017.06.009

Cited by 7 publications

(4 citation statements)

References 36 publications

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“…Impaired autophagy in glomerular and tubular cells has been recognized in the pathogenesis of DKD, contributing to the accumulation of cellular damage (29). A decreased expression of MAP1LC3A mRNA was described in the urinary sediment from patients with DKD (30), an opposite finding to what we observed in the present study for MAP1LC3C. However, it is not clear whether the three LC3 proteins have the same biological function in autophagy or in other pathways (28).…”

Section: Discussioncontrasting

confidence: 90%

Urinary Sediment Transcriptomic and Longitudinal Data to Investigate Renal Function Decline in Type 1 Diabetes

et al. 2020

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Section: Discussioncontrasting

confidence: 90%

Urinary Sediment Transcriptomic and Longitudinal Data to Investigate Renal Function Decline in Type 1 Diabetes

et al. 2020

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“…The beneficial effect of SGLT2i on fibrosis may be secondary to oxidative and organellar stress ( 99 ). In diabetic patients, autophagic proteins are decreased, and the levels correlate with the stage of CKD ( 106 , 107 ). Autophagia is important for the clearance of damaged proteins and organelles, and thus the prevention of inflammation ( 106 ).…”

Section: Resultsmentioning

confidence: 99%

Narrative review investigating the nephroprotective mechanisms of sodium glucose cotransporter type 2 inhibitors in diabetic and nondiabetic patients with chronic kidney disease

Speedtsberg,

Tepel

2023

Front. Endocrinol.

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Background and aimsOutcome trials using sodium glucose cotransporter type 2 inhibitors have consistently shown their potential to preserve kidney function in diabetic and nondiabetic patients. Several mechanisms have been introduced which may explain the nephroprotective effect of sodium glucose cotransporter type 2 inhibitors beyond lowering blood glucose. This current narrative review has the objective to describe main underlying mechanisms causing a nephroprotective effect and to show similarities as well as differences between proposed mechanisms which can be observed in patients with diabetic and nondiabetic chronic kidney disease.MethodsWe performed a narrative review of the literature on Pubmed and Embase. The research string comprised various combinations of items including “chronic kidney disease”, “sodium glucose cotransporter 2 inhibitor” and “mechanisms”. We searched for original research and review articles published until march, 2022. The databases were searched independently and the agreements by two authors were jointly obtained.ResultsSodium glucose cotransporter type 2 inhibitors show systemic, hemodynamic, and metabolic effects. Systemic effects include reduction of blood pressure without compensatory activation of the sympathetic nervous system. Hemodynamic effects include restoration of tubuloglomerular feedback which may improve pathologic hyperfiltration observed in most cases with chronic kidney disease. Current literature indicates that SGLT2i may not improve cortical oxygenation and may reduce medullar oxygenation.ConclusionSodium glucose cotransporter type 2 inhibitors cause nephroprotective effects by several mechanisms. However, several mediators which are involved in the underlying pathophysiology may be different between diabetic and nondiabetic patients.

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“…Autophagy protects cells from damage by eliminating damaged proteins and organelles. Clinically, blood and urine biomarkers of autophagic proteins are depressed in the patients with diabetic kidney disease [ 75 , 76 ], and renal biopsy specimens of patients with insulin resistance exhibit molecular evidence of autophagy suppression [ 77 ]. In this study, we found that autophagy was negatively correlated with the level of inflammation and ROS, which was similar to previous research results.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Allograft Inflammatory Factor-1 on Inflammation, Oxidative Stress, and Autophagy via miR-34a/ATG4B Pathway in Diabetic Kidney Disease

Hao

Xiaotian

Jie

et al. 2022

Oxidative Medicine and Cellular Longevity

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Increasing evidence suggests that disorders of inflammation, oxidative stress, and autophagy contribute to the pathogenesis of diabetic kidney disease (DKD). This study attempted to clarify the effect of allograft inflammatory factor-1 (AIF-1), miR-34a, and ATG4B on inflammation, oxidative stress, and autophagy in DKD both in vitro and in vivo experiments. In vivo, it was found that the levels of AIF-1, miR-34a, oxidative stress, and inflammatory factors were significantly increased in blood and urine samples of DKD patients and mouse models and correlated with the level of urinary protein. In vitro, it was also found that the expressions of AIF-1, miR-34a, ROS, and inflammatory factors were increased, while ATG4B and other autophagy related proteins were decreased in human renal glomerular endothelial cells (HRGECs) cultured with high concentration glucose medium (30 mmol/L). When AIF-1 gene was overexpressed, the levels of miR-34a, ROS, and inflammatory factors were significantly upregulated, and autophagy-related proteins such as ATG4B were downregulated, while downregulation of AIF-1 gene had the opposite effect. In addition, miR-34a inhibited the expression of ATG4B and autophagy-related proteins and increased the levels of ROS and inflammation. Furthermore, the result of luciferase reporter assay suggested that ATG4B was the target gene of miR-34a. When ATG4B gene was overexpressed, the level of autophagy was upregulated, and inflammatory factors were downregulated. Conversely, when ATG4B gene was inhibited, the level of autophagy was downregulated, and inflammatory factors were upregulated. Then, autophagy inducers inhibited the levels of inflammation and ROS, whereas autophagy inhibitors had the opposite function in HRGECs induced by glucose (30 mmol/L). In conclusion, the above data suggested that AIF-1 regulated the levels of inflammation, oxidative stress, and autophagy in HRGECs via miR-34a/ATG4B pathway to contribute to the pathogenesis of diabetic kidney disease.

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Evaluation of urinary autophagy transcripts expression in diabetic kidney disease

Cited by 7 publications

References 36 publications

Urinary Sediment Transcriptomic and Longitudinal Data to Investigate Renal Function Decline in Type 1 Diabetes

Urinary Sediment Transcriptomic and Longitudinal Data to Investigate Renal Function Decline in Type 1 Diabetes

Narrative review investigating the nephroprotective mechanisms of sodium glucose cotransporter type 2 inhibitors in diabetic and nondiabetic patients with chronic kidney disease

The Effect of Allograft Inflammatory Factor-1 on Inflammation, Oxidative Stress, and Autophagy via miR-34a/ATG4B Pathway in Diabetic Kidney Disease

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