Liquiritigenin, an Active Ingredient of Liquorice, Alleviates Acute Kidney Injury by VKORC1-Mediated Ferroptosis Inhibition.

Acute kidney injury (AKI) is a major public health problem worldwide that still lacks effective treatments. Recent studies have suggested that ferroptosis is a key mediator of AKI due to its activation of lipid peroxidation. Therefore, we hypothesized that antiferroptosis agents might be a novel potential therapeutic strategy for AKI.

ACSF2 and lysine lactylation contribute to renal tubule injury in diabetes.

Aims: Lactate accumulation is reported to be a biomarker for diabetic nephropathy progression. Lactate drives lysine lactylation, a newly discovered post-translational modification that is involved in the pathogenesis of cancers and metabolic and inflammatory disease. Here, we aimed to determine whether lysine lactylation is involved in the pathogenesis of diabetic nephropathy.

Mitochondria-associated endoplasmic reticulum membrane (MAM): a dark horse for diabetic cardiomyopathy treatment.

Diabetic cardiomyopathy (DCM), an important complication of diabetes mellitus (DM), is one of the most serious chronic heart diseases and has become a major cause of heart failure worldwide. At present, the pathogenesis of DCM is unclear, and there is still a lack of effective therapeutics. Previous studies have shown that the homeostasis of mitochondria and the endoplasmic reticulum (ER) play a core role in maintaining cardiovascular function, and structural and functional abnormalities in these organelles seriously impact the occurrence and development of various cardiovascular diseases, including DCM.

VDR Activation Attenuates Renal Tubular Epithelial Cell Ferroptosis by Regulating Nrf2/HO-1 Signaling Pathway in Diabetic Nephropathy.

Diabetic nephropathy (DN) is a serious microvascular complication of diabetes. Ferroptosis, a new form of cell death, plays a crucial role in the pathogenesis of DN. Renal tubular injury triggered by ferroptosis might be essential in this process.

Broadening horizons: the contribution of mitochondria-associated endoplasmic reticulum membrane (MAM) dysfunction in diabetic kidney disease.

Diabetic kidney disease (DKD) is a global health issue that presents a complex pathogenesis and limited treatment options. To provide guidance for precise therapies, it is crucial to accurately identify the pathogenesis of DKD. Several studies have recognized that mitochondrial and endoplasmic reticulum (ER) dysfunction are key drivers of the pathogenesis of DKD.

Broadening horizons: the multifaceted functions of ferroptosis in kidney diseases.

Ferroptosis is an iron-dependent programmed cell death pattern that is characterized by iron overload, reactive oxygen species (ROS) accumulation and lipid peroxidation. Growing viewpoints support that the imbalance of iron homeostasis and the disturbance of lipid metabolism contribute to tissue or organ injury in various kidney diseases by triggering ferroptosis. At present, the key regulators and complicated network mechanisms associated with ferroptosis have been deeply studied; however, its role in the initiation and progression of kidney diseases has not been fully revealed.

The Road from AKI to CKD: Molecular Mechanisms and Therapeutic Targets of Ferroptosis.

Acute kidney injury (AKI) is a prevalent pathological condition that is characterized by a precipitous decline in renal function. In recent years, a growing body of studies have demonstrated that renal maladaptation following AKI results in chronic kidney disease (CKD). Therefore, targeting the transition of AKI to CKD displays excellent therapeutic potential.

Emerging Role of Ferroptosis in Diabetic Kidney Disease: Molecular Mechanisms and Therapeutic Opportunities.

Diabetic kidney disease (DKD) is one of the most common and severe microvascular complications of diabetes mellitus (DM), and has become the leading cause of end-stage renal disease (ESRD) worldwide. Although the exact pathogenic mechanism of DKD is still unclear, programmed cell death has been demonstrated to participate in the occurrence and development of diabetic kidney injury, including ferroptosis. Ferroptosis, an iron-dependent form of cell death driven by lipid peroxidation, has been identified to play a vital role in the development and therapeutic responses of a variety of kidney diseases, such as acute kidney injury (AKI), renal cell carcinoma and DKD.

Quercetin Ameliorates Diabetic Kidney Injury by Inhibiting Ferroptosis via Activating Nrf2/HO-1 Signaling Pathway.

Diabetic nephropathy (DN) is thought to be the major cause of end-stage renal disease. Due to its complicated pathogenesis and the low efficacy of DN treatment, a deep understanding of new etiological factors may be useful. Ferroptosis, a nonapoptotic form of cell death, is characterized by the accumulation of iron-dependent lipid peroxides to lethal levels.

A Comprehensive Weighted Gene Co-expression Network Analysis Uncovers Potential Targets in Diabetic Kidney Disease.

Background And Objectives: Diabetic kidney disease (DKD) is one of the most common microvascular complications of diabetes. It has always been difficult to explore novel biomarkers and therapeutic targets of DKD. We aimed to identify new biomarkers and further explore their functions in DKD.

Ferroptosis: A new insight for treatment of acute kidney injury.

Acute kidney injury (AKI), one of the most prevalent clinical diseases with a high incidence rate worldwide, is characterized by a rapid deterioration of renal function and further triggers the accumulation of metabolic waste and toxins, leading to complications and dysfunction of other organs. Multiple pathogenic factors, such as rhabdomyolysis, infection, nephrotoxic medications, and ischemia-reperfusion injury, contribute to the onset and progression of AKI. However, the detailed mechanism remains unclear.

Effects of salvianolic acid A and salvianolic acid B in renal interstitial fibrosis via PDGF-C/PDGFR-α signaling pathway.

Background: Renal interstitial fibrosis (RIF) is the main pathological feature of end-stage renal disease (ESRD) caused by various chronic kidney diseases (CKD), and is closely related to renal dysfunction and patient prognosis. Salvianolic acid A (Sal A) and salvianolic acid B (Sal B), isolated from traditional Chinese medicine Salviae miltiorrhizae, have been confirmed to have anti-fibrotic effects on liver, cardiac and kidney. However, the precise molecular mechanism underlying the nephroprotective effects of Sal A and Sal B, and whether there is a difference between the two in RIF are still unclear.

Ferroptosis and Acute Kidney Injury (AKI): Molecular Mechanisms and Therapeutic Potentials.

Acute kidney injury (AKI), a common and serious clinical kidney syndrome with high incidence and mortality, is caused by multiple pathogenic factors, such as ischemia, nephrotoxic drugs, oxidative stress, inflammation, and urinary tract obstruction. Cell death, which is divided into several types, is critical for normal growth and development and maintaining dynamic balance. Ferroptosis, an iron-dependent nonapoptotic type of cell death, is characterized by iron overload, reactive oxygen species accumulation, and lipid peroxidation.

Mitochondrial dysfunction in diabetic tubulopathy.

Diabetic kidney disease (DKD) is a devastating microvascular complication associated with diabetes mellitus. Recently, the major focus of glomerular lesions of DKD has partly shifted to diabetic tubulopathy because of renal insufficiency and prognosis of patients is closely related to tubular atrophy and interstitial fibrosis. Indeed, the proximal tubule enriching in mitochondria for its high energy demand and dependence on aerobic metabolism has given us pause to focus primarily on the mitochondria-centric view of early diabetic tubulopathy.

cAMP-response element binding protein mediates podocyte injury in diabetic nephropathy by targeting lncRNA DLX6-AS1.

Background: Progressive proteinuria is one of the earliest clinical features of diabetic nephropathy (DN). In our previous study, lncRNA DLX6-AS1 (DLX6-AS1, Dlx6os1 in the mouse) was found to be associated with the extent of albuminuria in DN patients. Furthermore, the lack of Dlx6os1 was pivotal in switching off the inflammatory response in db/db mouse model.

miR-193a as a potential mediator of WT-1/synaptopodin in the renoprotective effect of Losartan on diabetic kidney.

Diabetic nephropathy (DN) is the most common complication of diabetic patients, and has become a global healthcare problem. In this study, we used diabetic mice to evaluate the effect of Losartan on DN, in which the experimental animals were divided into three groups: non-diabetic mice (db/m group), untreated-diabetic mice (db/db group), and Losartan-treated diabetic mice (db/db-losartan). Next, immunohistochemistry and immunofluorescence were used to detect Wilms tumor protein 1 (WT-1) and synaptopodin expression, respectively.

Diabetes Mellitus as a Risk Factor for Progression from Acute Kidney Injury to Acute Kidney Disease: A Specific Prediction Model.

Purpose: Acute kidney injury is very common in hospitalized patients and carries a significant risk of mortality. Although timely intervention may improve patient prognosis, studies on the development of acute kidney disease in patients with acute kidney injury remain scarce. Thus, we constructed a prediction model to identify patients likely to develop acute kidney disease.

MiR-138 plays an important role in diabetic nephropathy through SIRT1-p38-TTP regulatory axis.

Diabetic nephropathy (DN) is the main cause of chronic kidney disease (CKD) and is one of the most common and serious complications of diabetes mellitus (DM). Sirtuin 1 (SIRT1) and tristetraprolin (TTP) are two important protective factors in DN; however, the regulatory relationship between SIRT1 and TTP, and the underneath mechanism are interesting but still unclear. Identifying the key factors that regulate SIRT1 or TTP may be of great value to the understanding and treatment of the DN.

Development and Validation of a Nomogram Model to Predict Acute Kidney Disease After Nephrectomy in Patients with Renal Cell Carcinoma.

Purpose: To develop and validate a nomogram model to predict the occurrence of acute kidney disease (AKD) after nephrectomy.

Patients And Methods: A retrospective cohort including 378 patients with renal cell carcinoma (RCC) who had undergone radical or partial nephrectomy between March 2013 and December 2017 at the First Affiliated Hospital of Zhengzhou University was analyzed. Of these, patients who had undergone surgery in an earlier period of time formed the training cohort (n=265) for nomogram development, and those who had undergone surgery thereafter formed the validation cohort (n=113) to confirm the model's performance.

[Retracted] Glycogen synthase kinase‑3β is required for epithelial‑mesenchymal transition and barrier dysfunction in mouse podocytes under high glucose conditions.

Following the publication of the above article, the authors regret to report that they have encountered some difficulties in reproducing the results presented in Figs. 1 and 4 in their subsequent studies. Therefore, they have requested that the article be retracted on account of a lack of confidence in the presented data.

Author Correction: MC1R is dispensable for the proteinuria reducing and glomerular protective effect of melanocortin therapy.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Melanocortin therapy ameliorates podocytopathy and proteinuria in experimental focal segmental glomerulosclerosis involving a podocyte specific non-MC1R-mediated melanocortinergic signaling.

The clinical effectiveness of adrenocorticotropin in inducing remission of steroid-resistant nephrotic syndrome points to a steroidogenic-independent anti-proteinuric activity of melanocortins. However, which melanocortin receptors (MCR) convey this beneficial effect and if systemic or podocyte-specific mechanisms are involved remain uncertain. In vivo, wild-type (WT) mice developed heavy proteinuria and kidney dysfunction following Adriamycin insult, concomitant with focal segmental glomerulosclerosis (FSGS) and podocytopathy, marked by loss of podocin and synaptopodin, podocytopenia and extensive foot process effacement on electron microscopy.

GSK3β-mediated Keap1-independent regulation of Nrf2 antioxidant response: A molecular rheostat of acute kidney injury to chronic kidney disease transition.

Transition of acute kidney injury (AKI) to chronic kidney disease (CKD) represents an important cause of kidney failure. However, how AKI is transformed into CKD remains elusive. Following folic acid injury, mice developed AKI with ensuing CKD transition, featured by variable degrees of interstitial fibrosis and tubular cell atrophy and growth arrest.

Prevalence and risk factors of chronic kidney disease and diabetic kidney disease in Chinese rural residents: a cross-sectional survey.

We conducted a cross-sectional survey including 23869 participants and aimed to measure the prevalences of and risk factors for chronic kidney disease (CKD) and diabetic kidney disease (DKD) in a Chinese rural population. CKD and DKD status was defined according to the combination of estimated glomerular filtration rate (eGFR) and presence of albuminuria Participant completed a questionnaire involving life-style and relevant medical history, and the blood and urinary specimen were taken. The age- and gender- adjusted prevalences of CKD and DKD were calculated and risk factors associated with the presence of CKD and DKD were analyzed by logistic regression.