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UROLOGY, NEPHROLOGY AND ANDROLOGY (151 journals)                     

Showing 1 - 144 of 144 Journals sorted alphabetically
Actas Urológicas Españolas     Full-text available via subscription   (Followers: 1)
Actas Urológicas Españolas (English Edition)     Full-text available via subscription   (Followers: 1)
Advances in Chronic Kidney Disease     Hybrid Journal   (Followers: 15)
Advances in Urology     Open Access   (Followers: 13)
African Journal of Nephrology     Open Access   (Followers: 1)
African Journal of Urology     Open Access   (Followers: 7)
AJP Renal Physiology     Hybrid Journal   (Followers: 8)
Aktuelle Urologie     Hybrid Journal   (Followers: 4)
American Journal of Kidney Diseases     Hybrid Journal   (Followers: 53)
American Journal of Men's Health     Open Access   (Followers: 9)
American Journal of Nephrology     Full-text available via subscription   (Followers: 31)
Andrologia     Hybrid Journal   (Followers: 3)
Andrology     Hybrid Journal   (Followers: 5)
Andrology & Gynecology : Current Research     Hybrid Journal   (Followers: 4)
Andrology and Genital Surgery     Open Access   (Followers: 8)
Arab Journal of Nephrology and Transplantation     Open Access   (Followers: 2)
Arab Journal of Urology     Open Access   (Followers: 7)
Archives of Clinical Nephrology     Open Access   (Followers: 2)
Archivio Italiano di Urologia e Andrologia     Open Access   (Followers: 1)
Archivos Españoles de Urología     Open Access   (Followers: 1)
Asian Journal of Andrology     Open Access   (Followers: 1)
Asian Journal of Urology     Open Access   (Followers: 3)
Asian Pediatric Nephrology Association     Open Access   (Followers: 3)
Bangladesh Journal of Urology     Open Access   (Followers: 5)
Basic and Clinical Andrology     Open Access  
BJU International     Hybrid Journal   (Followers: 19)
BJUI Compass     Open Access   (Followers: 1)
BMC Nephrology     Open Access   (Followers: 9)
BMC Urology     Open Access   (Followers: 13)
Canadian Journal of Kidney Health and Disease     Open Access   (Followers: 7)
Canadian Urological Association Journal     Open Access   (Followers: 1)
Cancer Urology     Open Access   (Followers: 1)
Cardiorenal Medicine     Full-text available via subscription   (Followers: 1)
Case Reports in Nephrology     Open Access   (Followers: 6)
Case Reports in Nephrology and Dialysis     Open Access   (Followers: 8)
Case Reports in Urology     Open Access   (Followers: 11)
Clinical and Experimental Nephrology     Hybrid Journal   (Followers: 5)
Clinical Journal of the American Society of Nephrology     Full-text available via subscription   (Followers: 24)
Clinical Kidney Journal     Open Access   (Followers: 5)
Clinical Medicine Insights : Urology     Open Access   (Followers: 3)
Clinical Nephrology     Full-text available via subscription   (Followers: 8)
Cuadernos de Cirugía     Open Access  
Current Opinion in Nephrology & Hypertension     Hybrid Journal   (Followers: 12)
Current Opinion in Urology     Hybrid Journal   (Followers: 11)
Current Urology     Open Access   (Followers: 10)
Current Urology Reports     Hybrid Journal   (Followers: 5)
Der Nephrologe     Hybrid Journal  
Der Urologe     Hybrid Journal   (Followers: 1)
Diabetic Nephropathy     Open Access  
EMC - Urología     Full-text available via subscription  
Enfermería Nefrológica     Open Access   (Followers: 1)
European Urology     Hybrid Journal   (Followers: 23)
European Urology Focus     Hybrid Journal   (Followers: 4)
European Urology Oncology     Hybrid Journal  
European Urology Open Science     Open Access   (Followers: 8)
Forum Nefrologiczne     Full-text available via subscription  
Geriatric Nephrology and Urology     Hybrid Journal   (Followers: 7)
Giornale di Clinica Nefrologica e Dialisi     Open Access  
Hellenic Urology     Open Access   (Followers: 3)
IJU Case Reports     Open Access  
Indian Journal of Nephrology     Open Access   (Followers: 2)
Indian Journal of Urology     Open Access   (Followers: 5)
International Brazilian Journal of Urology     Open Access   (Followers: 5)
International Journal of Nephrology     Open Access   (Followers: 2)
International Journal of Nephrology and Renovascular Disease     Open Access   (Followers: 2)
International Journal of Urology     Hybrid Journal   (Followers: 10)
International Urology and Nephrology     Hybrid Journal   (Followers: 6)
Journal für Urologie und Urogynäkologie/Österreich     Hybrid Journal  
Journal of Clinical Nephrology     Open Access   (Followers: 1)
Journal of Clinical Urology     Hybrid Journal   (Followers: 12)
Journal of Endoluminal Endourology     Open Access  
Journal of Endourology     Hybrid Journal   (Followers: 2)
Journal of Endourology Case Reports     Hybrid Journal  
Journal of Genital System & Disorders     Hybrid Journal   (Followers: 1)
Journal of Integrative Nephrology and Andrology     Open Access   (Followers: 2)
Journal of Kidney Cancer and VHL     Open Access  
Journal of Lower Genital Tract Disease     Hybrid Journal  
Journal of Nephrology     Hybrid Journal   (Followers: 5)
Journal of Nephrology Research     Open Access   (Followers: 2)
Journal of Pediatric Nephrology     Open Access   (Followers: 3)
Journal of Renal Care     Hybrid Journal   (Followers: 8)
Journal of Renal Nursing     Full-text available via subscription   (Followers: 8)
Journal of Renal Nutrition     Hybrid Journal   (Followers: 28)
Journal of Renal Nutrition and Metabolism     Open Access   (Followers: 2)
Journal of the American Society of Nephrology     Full-text available via subscription   (Followers: 38)
Journal of The Egyptian Society of Nephrology and Transplantation     Open Access  
Journal of Urology & Nephrology     Open Access  
Kidney Diseases     Open Access   (Followers: 3)
Kidney International     Hybrid Journal   (Followers: 52)
Kidney International Reports     Open Access   (Followers: 6)
Kidney Medicine     Open Access   (Followers: 1)
Kidney Research Journal     Open Access   (Followers: 6)
Kidneys (Počki)     Open Access  
Nature Reviews Nephrology     Full-text available via subscription   (Followers: 29)
Nature Reviews Urology     Full-text available via subscription   (Followers: 9)
Nefrología     Open Access  
Nefrología (English Edition)     Open Access  
Nephro-Urology Monthly     Open Access   (Followers: 1)
Nephrology     Hybrid Journal   (Followers: 13)
Nephrology Dialysis Transplantation     Hybrid Journal   (Followers: 26)
Nephron     Hybrid Journal   (Followers: 3)
Nephron Clinical Practice     Full-text available via subscription   (Followers: 3)
Nephron Experimental Nephrology     Full-text available via subscription   (Followers: 4)
Nephron Extra     Open Access   (Followers: 1)
Nephron Physiology     Full-text available via subscription   (Followers: 4)
Neurourology and Urodynamics     Hybrid Journal   (Followers: 1)
OA Nephrology     Open Access   (Followers: 2)
Open Access Journal of Urology     Open Access   (Followers: 6)
Open Journal of Nephrology     Open Access   (Followers: 4)
Open Journal of Urology     Open Access   (Followers: 6)
Open Urology & Nephrology Journal     Open Access  
Paediatric Nephrology Journal of Bangladesh     Open Access   (Followers: 4)
Portuguese Journal of Nephrology & Hypertension     Open Access   (Followers: 1)
Progrès en Urologie     Full-text available via subscription  
Progrès en Urologie - FMC     Full-text available via subscription  
Prostate Cancer and Prostatic Diseases     Hybrid Journal   (Followers: 4)
Renal Failure     Open Access   (Followers: 11)
Renal Replacement Therapy     Open Access   (Followers: 3)
Research and Reports in Urology     Open Access   (Followers: 4)
Revista de Nefrología, Diálisis y Trasplante     Open Access   (Followers: 1)
Revista Mexicana de Urología     Open Access  
Revista Urologia Colombiana     Open Access  
Scandinavian Journal of Urology     Hybrid Journal   (Followers: 6)
Seminars in Nephrology     Hybrid Journal   (Followers: 11)
The Prostate     Hybrid Journal   (Followers: 6)
Therapeutic Advances in Urology     Open Access   (Followers: 3)
Translational Research in Urology     Open Access   (Followers: 1)
Trends in Urology & Men's Health     Partially Free   (Followers: 1)
Urine     Open Access  
Uro-News     Hybrid Journal  
Urolithiasis     Hybrid Journal   (Followers: 1)
Urologia Internationalis     Full-text available via subscription   (Followers: 1)
Urologia Journal     Hybrid Journal  
Urologic Clinics of North America     Full-text available via subscription   (Followers: 3)
Urologic Nursing     Full-text available via subscription   (Followers: 3)
Urological Science     Open Access  
Urologicheskie Vedomosti     Open Access  
Urologie in der Praxis     Hybrid Journal  
Urology     Hybrid Journal   (Followers: 26)
Urology Case Reports     Open Access   (Followers: 3)
Urology Times     Free   (Followers: 3)
Urology Video Journal     Open Access  
World Journal of Nephrology and Urology     Open Access   (Followers: 5)
World Journal of Urology     Hybrid Journal   (Followers: 10)

           

Similar Journals
Journal Cover
Diabetic Nephropathy
Number of Followers: 0  

  This is an Open Access Journal Open Access journal
ISSN (Online) 2719-3500
Published by Sciendo Homepage  [370 journals]
  • The role of vitamin D receptor agonist on podocyte injury induced by high
           glucose

    • Abstract: BackgroundThe effects of vitamin D receptor (VDR) agonist paricalcitol on the podocyte injury induced by high glucose (HG) were investigated in conditioned immortalized mouse podocytes (MPC-5).Methods(1) Grouped according to different glucose concentrations: normal group (NG): 5.6 mmol/L glucose; HG stimulation group: 25 mmol/L glucose (25HG); high osmotic control group (NG + M): 5.6 mmol/L glucose + 19.4 mmol/L D-mannitol. The expression levels of VDR, podocyte marker proteins podocin, nephrin and mesenchymal marker proteins α-smooth muscle actin (α-SMA), matrix metalloproteinases (MMP9) in MPC-5 were measured, respectively. (2) Effect of VDR agonist-paricalcitol on podocyte epithelial-mesenchymal transition (EMT) induced by HG: cultured podocytes are divided into NG group, NG with dimethylsulfoxide (DMSO) group (NG+D), NG with paricalcitol (0.1 μmol/L) group (NG+P), HG group, HG with DMSO group (HG+D), and HG with paricalcitol (0.1 μmol/L) group (HG+P). The expression levels of VDR, podocyte marker proteins, marker proteins of mesenchymal cells, and the albumin flow in each group were then detected.Results(1) Under HG conditions, the expressions of VDR, podocin, and nephrin were decreased, while the expressions of α-SMA and MMP9 were increased (all P < 0.05). After administration of paricalcitol, the levels of VDR, podocin, and nephrin were increased, while the expressions of α-SMA and MMP9 were decreased compared with the control groups (all P < 0.05). (2) The results of albumin flow showed that the albumin flow of podocytes increased under the condition of HG, while it decreased after the treatment of paricalcitol.ConclusionThe podocyte injury induced by HG could be partly rescued by Paricalcitol.
      PubDate: Mon, 01 Aug 2022 00:00:00 GMT
       
  • TGF-β signaling in diabetic nephropathy: An update

    • Abstract: Diabetic nephropathy (DN) is a common complication in patients with diabetes and the leading cause of end-stage renal disease. Accumulating evidence shows that transforming growth factor beta-1 (TGF-β1) is a key mediator in the pathogenesis of DN. TGF-β1 binds to its receptors to activate canonical and noncanonical downstream signaling pathways to exert its biological activities. Among them, canonical Smad signaling is the major pathway responsible for the development of DN. In addition to TGF-β1, many stress molecules, such as advanced glycation end products (AGEs), angiotensin II (Ang II), and C-reactive protein (CRP), can also activate Mothers against decapentaplegic homologs (Smads) via the extracellular signal-regulated kinase (ERK)/p38 mitogen-activated protein kinase (MAPK) cross talk mechanism. Furthermore, TGF-β/Smad signaling can also cross talk with nuclear factor kappa B (NF-κB) signaling to regulate renal inflammation via the induction of IκBα by Smad7. In the context of renal fibrosis, Smad3 is pathogenic, while Smad2 and Smad7 are protective. TGF-β signaling also upregulates the pathogenic microRNAs (miRNAs) (namely, miR-21, miR-192, and miR-377) and long noncoding RNAs (lncRNAs) (namely, Erbb4-IR (intron region, IR), LncRNA9884, and Arid2-IR) but downregulates the protective miRNAs (namely, miR-29a/b and miR-200a) to mediate DN. Thus, targeting TGF-β signaling, either by blocking its ligand, its receptor (i.e., TGF-β receptor-2 [TGFBR2]), Smad3, and downstream miRNAs/lncRNAs or by overexpressing Smad7, has been shown to improve DN. In addition, pharmaceutically targeting TGF-β signaling using chemical inhibitors and traditional Chinese medicine (TCM), including Tangshen formula, Chaihuang-Yishen granule, and herbal extracts (berberine, asiatic acid, and naringenin), also shows renoprotective effect in diabetes. In summary, TGF-β signaling is a critical pathway leading to DN and may be a therapeutic target for combating DN.
      PubDate: Wed, 29 Jun 2022 00:00:00 GMT
       
  • Renal biopsy in patients with diabetes: Yesterday, today, and tomorrow

    • PubDate: Thu, 16 Jun 2022 00:00:00 GMT
       
  • Insulin therapy in diabetic kidney disease

    • Abstract: Diabetic kidney disease (DKD) is the main cause of end-stage renal disease (ESRD). The use of insulin represents a challenge in patients with DKD due to the patient and medication issues. Insulin regimens, insulin dosing, and titration need to be individualized based on the patient's age, renal function, and comorbidities to improve glycemic control and reduce the risk of hypoglycemia. Insulin is the primary treatment in all patients with type 1 diabetes mellitus (T1DM) and DKD. For patients with type 2 diabetes mellitus (T2DM) and early stage of DKD, basal insulin combined with oral antidiabetic drugs (OADs) is recommended. In patients with middle and advanced DKD, it is necessary to adjust the dose of insulin according to stages of DKD, and the use of insulin analogs is recommended. In particular, elderly patients with DKD can simplify their insulin regimen to reduce the risk of hypoglycemia. In pregnant women with DKD, insulin requirements also vary based on parity and the stage of pregnancy.
      PubDate: Thu, 16 Jun 2022 00:00:00 GMT
       
  • Analysis of dapagliflozin-induced expression profile of long noncoding
           RNAs in proximal tubular epithelial cells of diabetic kidney disease

    • Abstract: BackgroundAccumulating evidence indicates that long noncoding RNAs (lncRNAs) play an important role in diabetic kidney disease (DKD). Dapagliflozin (DAPA), a sodium-glucose cotransporter 2 (SGLT2) inhibitor, exerts protective effects against DKD, but the underlying mechanism remains unclear.MethodsIn this study, we performed RNA microarray analysis to investigate differentially expressed lncRNAs and mRNAs in human proximal tubular epithelial cells (HK-2 cells) cultured with normal glucose (Ng), high glucose (Hg), and Hg plus DAPA, and conducted bioinformatic analyses to investigate their functions.ResultsCompared with the Ng group, 6761 lncRNAs and 3162 mRNAs were differentially expressed in the Hg group. Expression levels of 714 and 259 lncRNAs were up- and down-regulated, respectively, whereas those of 138 and 127 mRNAs were up- and down-regulated, respectively, after DAPA treatment (fold change ≥2, P < 0.05). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted to assess the biological functions of lncRNAs and potential target genes. According to GO analysis, dysregulated mRNAs were primarily enriched in the cell cycle, whereas DAPA-induced mRNAs were enriched in collagen biosynthesis and regulation of programmed cell death. Type I diabetes mellitus and cell cycle signaling were the main KEGG pathways in the Hg group. However, cancer and signal transduction pathways were related to DAPA treatment.ConclusionsFinally, we established protein–protein interaction (PPI) networks, as well as lncRNA–mRNA and lncRNA–miRNA–mRNA networks, and identified five potentially important lncRNAs whose expression levels were altered by DAPA treatment. Our findings suggest that lncRNAs are potential targets for DKD treatment.
      PubDate: Thu, 16 Jun 2022 00:00:00 GMT
       
  • Renoprotective mechanisms of SGLT2 inhibitor in diabetic kidney disease

    • Abstract: Diabetic kidney disease (DKD), as the primary cause of end-stage renal disease (ESRD), is becoming a growing public health challenge worldwide. Early intervention in conditions involving high glucose levels will prevent the progression of DKD. Sodium-glucose cotransporter 2 inhibitors (SGLT2is) comprise a new class of medications used to reduce hyperglycemia in patients with diabetes by inhibiting renal reabsorption of filtered glucose. Interestingly, SGLT2i is not only capable of controlling the blood glucose level but also has other benefits in terms of blood pressure control, body weight decrease, and albuminuria reduction. It is assumed that various events, such as energy metabolism disorder, insulin resistance, glomerular hyperfiltration, oxidative stress, inflammation, and fibrosis, attributable to the pathogenesis of DKD, can be improved by SGLT2i. Clinical trials have demonstrated that SGLT2i can exert renoprotective effects and reduce the morbidity and mortality due to ESRD. In this review, we focus on the most recent findings from clinical trials and the underlying mechanisms by which SGLT2 inhibitors afford renal protection.
      PubDate: Fri, 10 Jun 2022 00:00:00 GMT
       
  • Emerging role of macrophages in diabetic nephropathy

    • Abstract: Increasing evidence shows that diabetic nephropathy is associated with immune disorder. Macrophages are a key immune cell infiltrating the kidney in both patients and experimental animal models of diabetes, and correlate with progressive renal injury under diabetic conditions. Blockade of renal macrophage infiltration by either genetic deletion or pharmacological inhibition has been shown to improve diabetic renal injury, revealing a pathogenic role of macrophages in diabetic nephropathy. Further, studies identify that M1 macrophages are a key player responsible for diabetic renal injury by triggering renal inflammation, while M2 macrophages are highly heterogenous, and may play diverse roles in either initiating the renal repairing process if renal inflammation is resolved, or promoting progressive renal fibrosis via a macrophage-to-myofibroblast transition (MMT) process if renal inflammation is ongoing. Macrophages may also interact with intrinsic kidney cells to mediate renal inflammation or fibrosis directly or indirectly by producing a variety of proinflammatory cytokines/chemokines and growth factors, or by macrophage-derived exosomes. In summary, macrophages are immunologically important in the pathogenesis of diabetic kidney disease and may play a driving role in the progression of diabetic nephropathy. Targeting macrophages may thus be considered as a novel therapy for combatting diabetic nephropathy.
      PubDate: Mon, 16 May 2022 00:00:00 GMT
       
  • Pyridoxamine alleviates high glucose induced fibrosis in renal tubular
           epithelial cell by inhibiting the activity of TGF-β1/Smad3 signaling
           pathway

    • Abstract: BackgroundRenal fibrosis is one of the main characteristics of diabetic nephropathy. TGF-β1/Smad3 pathway is expected to reveal the pathogenesis of renal fibrosis in diabetic nephropathy (DN). Pyridoxamine (PM), a natural form of vitamin B6, is a powerful inhibitor of advanced glycation end products (AGEs). PM plays an anti-apoptotic, anti-oxidative stress, and fibrosis role in DN. The purpose of this study was to assess whether PM has a protective effect in renal tubular epithelial and to investigate its possible mechanism.MethodsThe effects of PM were investigated in HK-2 cells induced by high glucose. HK-2 cells were administered with PM at a dose of 1 mmol/L. Western blot and Realtime PCR were used to detect the expression levels of renal fibrosis related proteins. The possible mechanism of PM was examined by expression of transforming growth factor-β1 (TGF-β1)/Smad3 pathway.ResultsPM could reduce the expression of Fibronectin (FN) and α-smooth muscle actin (α-SMA) induced by high glucose. PM could also affect the activity of TGF-β1/Smad3 pathway in HK-2 cells. FN and α-SMA were up-regulated by overexpression of Smad3 for 48 h. After adding PM, the levels of FN and α-SMA are significantly decreased.ConclusionOur findings indicate that PM showed a protective effect in HK-2 cells through the inhibition of TGF-β1/Smad3 pathway.
      PubDate: Sat, 30 Apr 2022 00:00:00 GMT
       
  • Diabetic nephropathy with crescent: A case report

    • Abstract: Diabetic nephropathy is one of the main complications of diabetes, and is also one of the important causes of end-stage renal disease. It is characterized by pathological changes such as thickening of the glomerular basement membrane, expansion of the mesangial matrix, glomerular sclerosis, and hyalinosis of small arteries. However, diabetic nephropathy is rarely accompanied by the formation of a large number of crescents. At this time, renal puncture is required to search for the cause in diabetic nephropathy with worsening renal function. We report a case of diabetic nephropathy with the formation of a large number of crescents.
      PubDate: Tue, 26 Apr 2022 00:00:00 GMT
       
  • Diabetic kidney disease, a potentially serious issue resulting from
           collision of the Covid-19 and diabetes global pandemics

    • PubDate: Fri, 01 Apr 2022 00:00:00 GMT
       
  • Diabetic nephropathy patient with heavy proteinuria: A case report

    • Abstract: The classical progression of diabetic kidney disease (DKD) is deterioration of renal function over decades. We reported a 53-year-old man with hypertension and heavy proteinuria who suffered rapid progression of DKD.
      PubDate: Mon, 21 Mar 2022 00:00:00 GMT
       
  • Foreword

    • PubDate: Wed, 25 Aug 2021 00:00:00 GMT
       
  • Pathogenesis of diabetic kidney disease

    • Abstract: Diabetic kidney disease (DKD) is characterized by an accumulation of extracellular matrix proteins such as collagen and fibronectin in the kidney, resulting in tubulointerstitial fibrosis, glomerular mesangial hypertrophy and expansion, thickening of the glomerular basement membrane, podocyte foot process effacement, and inflammation due to the infiltration of monocytes and macrophages. All of these factors contribute to kidney function loss and can ultimately lead to progressive chronic kidney disease and kidney failure. In the review, we summarize the current state of knowledge in the pathogenesis of diabetic kidney disease to include the impact of genetic and environmental factors, hemodynamic changes, glycemic control, inflammation, proteinuria and novel mechanisms such as non-coding RNAs and lipotoxicity.
      PubDate: Wed, 25 Aug 2021 00:00:00 GMT
       
  • The expression of POMC and AgRP in brain and kidney tissues at different
           stages of diabetic nephropathy rats

    • Abstract: ObjectiveTo explore the changes of proopiomelanocortin (POMC) and Agouti-Related Peptide (AgRP) expression in brain and kidney tissues under insulin intervention at different stages of diabetic nephropathy (DN) rats.MethodsThe male Sprague-Dawley (SD) rats of DN were treated with high-fat diet for 8 weeks and induced by intraperitoneally injection of streptozotocin (30 mg/kg) for one time. Then DN rats were also injected insulin subcutaneously at 2–5 U/(kg·24 h) from initiation of the streptozotocin. Kidney tissue, blood sample, and 24 h-urine were collected to detect the ratio of kidney/body weight, blood glucose and 24-h urinary albumin excretion rate at different stages (4, 8, 12, and 16 weeks). Immunohistochemistry assay was used to measure the expression of POMC and AgRP at different stages of DN rats.ResultsThe DN rats were established successfully. With the progression of DN, blood glucose, 24-h urinary albumin excretion rate and kidney body weight ratio increased significantly, while decreased when insulin was injected. Immunohistochemistry showed that the expression levels of POMC were decreased gradually in brain and kidney tissues. Conversely, the expression of AgRP in kidney was highest at week 8 and then decreased gradually. The effect of insulin on normalizing POMC and AgRP expression in brain and renal tissues was also observed in DKD rats.ConclusionWith the progression of DN, the expression of POMC and AgRP in kidney tissues was observed at different stages of disease, and their expressions were significantly normalized by insulin. The mechanism of in situ expression of POMC and AGRP in kidney to the progression of DN needs further investigations.
      PubDate: Wed, 25 Aug 2021 00:00:00 GMT
       
  • Sitagliptin ameliorates ER stress in diabetic kidney disease through
           upregulation of SIRT1

    • Abstract: ObjectivesEndoplasmic reticulum (ER) stress plays a significant role in the progression of diabetic kidney disease (DKD), and dipeptidyl peptidase-4 (DPP4) inhibitors are widely used antihyperglycemic agents, exerting renal beneficial effects in DKD. Here, we investigated the role of DPP4 inhibitor Sitagliptin (Sita) in ER homeostasis in the kidneys of diabetic DBA2/J (D2) mice and in albumin-stimulated HK-2 cells.Methods and ResultsER stress was observed both in vivo and in vitro, as reflected by notably increased glucose-regulated protein of 78 kDa (GRP78), CHOP, high phosphorylation of PERK (p-PERK), and cleaved caspase3 (c-CASP3), whereas Sita effectively attenuated these disorders. Meanwhile, Sita increased the expression of SIRT1 both in vivo and in vitro. To further validate the potential effects of SIRT1 in regulating ER stress, we regulated SIRT1 by siRNA and overexpressed plasmids in albumin-overloaded HK-2 cells. Elevated SIRT1 alleviated albumin-induced ER stress, while decreased SIRT1 further aggravated ER stress in albumin-treated HK-2 cells.ConclusionThe results suggest that a novel mechanism links the DPP4 enzyme to ER stress during tubular injury in DKD and highlight that SIRT1 may be a potential target for managing DKD.
      PubDate: Wed, 25 Aug 2021 00:00:00 GMT
       
  • Inaugural Statement

    • PubDate: Wed, 25 Aug 2021 00:00:00 GMT
       
  • A point mutation of mitochondrial genes in diabetes and deafness with
           focal segmental glomerular sclerosis

    • Abstract: Deafness, diabetes and proteinuria are typically understood to be an uncommon combination. Here, we reported a 26-year-old woman with a history of persistent deafness, diabetes mellitus, and proteinuria. The diagnosis mainly depends on clinical symptoms, but the cause of the disease should be examined. The histological finding in renal biopsy showed secondary focal segmental glomerular sclerosis (FSGS), but not classic diabetic nephropathy. Further pathogeny was found. Subsequently, a 3243A>G mutation in the mitochondrial DNA was found. Thus, the diagnosis of maternally inherited deafness and diabetes (MIDD) was considered. Ineffective and unnecessary immunosuppression can be avoided through timely diagnosis. Long-term treatment of CoQ10 can be useful in MIDD patients.
      PubDate: Wed, 25 Aug 2021 00:00:00 GMT
       
  • The multifaceted contributions of long noncoding RNAs on mitochondrial
           dysfunction in diabetic nephropathy

    • PubDate: Wed, 25 Aug 2021 00:00:00 GMT
       
  • NRF2: A potential target for the treatment of diabetic nephropathy

    • Abstract: One of the major complications of diabetes mellitus is diabetic nephropathy (DN), the pathogenesis of which is primarily driven by oxidative stress. As a major regulator of antioxidant responses, the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) has recently attracted much interest. NRF2 is a primary defense mechanism against the cytotoxic effects of oxidative stress, involving heterogeneous detoxification, the production of antioxidants and anti-inflammatory molecules, DNA repair, nuclear chaperones, and proteasome systems. A myriad of studies in pre-clinical models of DN have consistently demonstrated a beneficial effect of NRF2 activation, suggesting that NRF2 is likely a promising target for treating DN. This has been further supported by findings from clinical trials of bardoxolone methyl, an activator of NRF2, despite the unexpected adverse cardiovascular effects. This review summarizes the support for therapeutic targeting of NRF2 in DN and emphasizes the need for the optimization of NRF2-based treatment with the minimization of potential adverse effects.
      PubDate: Wed, 25 Aug 2021 00:00:00 GMT
       
  • Key profibrotic and pro-inflammatory pathways in the pathogenesis of
           diabetic kidney disease

    • Abstract: Diabetes is a noncommunicable disease and arguably represents the greatest pandemic in human history. Diabetic kidney disease (DKD) is seen in both type 1 and type 2 diabetes and can be detected in up to 30–50% of diabetic subjects. DKD is a progressive chronic kidney disease (CKD) and is a leading cause of mortality and morbidity in patients with diabetes. Renal fibrosis and inflammation are the major pathological features of DKD. There are a large number of independent and overlapping profibrotic and pro-inflammatory pathways involved in the pathogenesis and progression of DKD. Among these pathways, the transforming growth factor-β (TGF-β) pathway plays a key pathological role by promoting fibrosis. Sirtuin-1 (SIRT1) is a protein deacetylase that has been shown to be renoprotective with an anti-inflammatory effect. It is postulated that a reduction in renal SIRT1 levels could play a key role in the pathogenesis of DKD and that restoration of SIRT1 will attenuate DKD. Cell division autoantigen 1 (CDA1) synergistically enhances the profibrotic effect of TGF-β in DKD by regulating the expression of the TGF-β type I receptor (TβRI). CDA1 has also been found to be an inhibitor of SIRT1 in the DNA damage response. Indeed, targeting CDA1 in experimental DKD not only attenuates diabetes-associated renal fibrosis but also attenuates the expression of key pro-inflammatory genes such as tumor necrosis factor-α (TNF-α) and Monocyte Che moattractant Protein-1 (MCP-1). In conclusion, there is a large body of experimental data to support the view that targeting CDA1 is a superior approach to directly targeting TGF-β in DKD since it is not only safe but also efficacious in retarding both fibrosis and inflammation.
      PubDate: Wed, 25 Aug 2021 00:00:00 GMT
       
 
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