Publications by authors named "Wenni Dai"

Obesity-related glomerulopathy (ORG) is an independent risk factor for chronic kidney disease and even progression to end-stage renal disease. Efforts have been undertaken to elucidate the mechanisms underlying the development of ORG and substantial advances have been made in the treatment of ORG, but relatively little is known about cell-specific changes in gene expression. To define the transcriptomic landscape at single-cell resolution, we analyzed kidney samples from four patients with ORG and three obese control subjects without kidney disease using single-cell RNA sequencing.

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Background: CAMK1 has been shown to be involved in human disease progression via regulating mitochondrial dynamics. However, whether CAMK1 mediates mitochondrial dynamics to regulate diabetic nephropathy (DN) process remains unclear.

Methods: Mice were injected with streptozotocin (STZ) to mimic diabetic mice models in vivo, and mice with proximal tubule-specific knockout of CAMK1 (CAMK1-KO) were generated.

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As a metabolic disorder, obesity can cause secondary kidney damage, which is called obesity-related glomerulopathy (ORG). As the incidence of obesity increases worldwide, so does the incidence of end-stage renal disease (ESRD) caused by ORGs. However, there is still a lack of effective strategies to prevent and delay the occurrence and development of ORG.

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Kidney disease has become a serious public health problem throughout the world, and its treatment and management constitute a huge global economic burden. Currently, the main clinical treatments are not sufficient to cure kidney diseases. During its development, nanotechnology has shown unprecedented potential for application to kidney diseases.

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Diabetic kidney disease (DKD) is the main complication in diabetes mellitus (DM) and the main cause of end-stage kidney disease worldwide. However, sodium glucose cotransporter 2 (SGLT2) inhibition, glucagon-like peptide-1 (GLP-1) receptor agonist, mineralocorticoid receptor antagonists and endothelin receptor A inhibition have yielded promising effects in DKD, a great part of patients inevitably continue to progress to uremia. Newly effective therapeutic options are urgently needed to postpone DKD progression.

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Diabetic kidney disease (DKD) is a major complication of diabetes mellitus (DM) and the leading cause of end-stage kidney disease (ESKD) worldwide. A significant number of drugs have been clinically investigated for the treatment of DKD. However, a large proportion of patients still develop end-stage kidney disease unstoppably.

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Diabetic kidney disease (DKD) is the predominant complication of diabetes mellitus (DM) and the leading cause of chronic kidney disease and end-stage renal disease worldwide, which are major risk factors for death. The pathogenesis of DKD is very complicated, including inflammation, autophagy impairment, oxidative stress, and so on. Recently, accumulating evidence suggests that the loss of mitochondrial quality control exerts critical roles in the progression of DKD.

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Background: Acute kidney injury (AKI), when occurring in diabetic kidney disease (DKD), is known to be more severe and difficult to recover from. Inflammation and apoptosis may contribute to the heightened sensitivity of, and non-recovery from, AKI in patients with DKD. Resolvin D1 (RvD1) is a potent lipid mediator which can inhibit the inflammatory response and apoptosis in many diseases.

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Diabetic kidney disease (DKD), as the main complication of diabetes mellitus, is the primary cause of the end-stage renal disease (ESRD) and the most common chronic kidney disease. Overall, 30-40% of patients with type 1 and type 2 diabetes eventually develop DKD. Although some diabetes patients have intensified glycemic control, they still develop diabetic kidney disease.

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