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PubMed Journals Articles About "Apelin Involved Progression Diabetic Nephropathy Inhibiting Autophagy Podocytes" RSS

19:17 EDT 22nd September 2018 | BioPortfolio

Apelin Involved Progression Diabetic Nephropathy Inhibiting Autophagy Podocytes PubMed articles on BioPortfolio. Our PubMed references draw on over 21 million records from the medical literature. Here you can see the latest Apelin Involved Progression Diabetic Nephropathy Inhibiting Autophagy Podocytes articles that have been published worldwide.

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Showing "Apelin involved progression diabetic nephropathy inhibiting autophagy podocytes" PubMed Articles 1–25 of 15,000+

Mangiferin prevents diabetic nephropathy progression and protects podocyte function via autophagy in diabetic rat glomeruli.

Diabetic nephropathy (DN) is one of the most severe microangiopathies of diabetes mellitus and is a leading cause of end stage renal disease. Numerous studies suggest that podocyte injury contributes to progressive proteinuria. Podocytes are highly specialized, terminally differentiated cells that are unable to proliferate, autophagy plays a key role in maintaining the structure and function of podocytes. Autophagy impairment is involved in the pathogenesis of podocyte loss, which leads to massive proteinur...


Astragaloside suppresses apoptosis of the podocytes in rats with diabetic nephropathy via miR-378/TRAF5 signaling pathway.

Apoptosis of podocytes plays a crucial role in diabetic nephropathy (DN) development, and astragaloside (AS-IV) has a significant impact on podocyte apoptosis. This study aims to explore the effect of AS-IV on diabetic nephropathy progression.

Apelin impairs myogenic response to induce diabetic nephropathy in mice.

The cause of the invalid reaction of smooth muscle cells to mechanical stimulation that results in a dysfunctional myogenic response that mediates the disruption of renal blood flow (RBF) in diabetic patients is debatable. The present study revealed that increased apelin concentration in serum of diabetic mice neutralized the myogenic response mediated by apelin receptor (APJ) and resulted in increased RBF, which promoted the progression of diabetic nephropathy. The results showed that apelin concentration,...


Mapping Txnip: Key connexions in progression of diabetic nephropathy.

Studies demonstrates the major involvement of inflammatory and apoptotic pathway in the pathophysiology of diabetic nephropathy. The cross talk between inflammatory and apoptotic pathway suggests Txnip as a molecular connexion in progression of disease state. Txnip modulates inflammatory pathway (via ROS production and NLRP3 inflammasome activity) and apoptotic pathway (via mTOR pathway). The key contribution of Txnip in both the pathways, reflects, its crucial role in diabetic nephropathy. In the present r...

Advances in early biomarkers of diabetic nephropathy.

Diabetic nephropathy is the main cause of chronic kidney disease, and represents the most common and serious complication of diabetes. The exact pathogenesis is complex and not elucidated. Several factors and mechanisms contribute to the development and outcome of diabetic nephropathy. An early diagnosis and intervention may slow down disease progression. A variety of biological markers associated with diabetic nephropathy were found in recent years, which was important for predicting the occurrence and dev...

Relationship Between the Brain Natriuretic Peptide (BNP) Level and Prognosis of Diabetic Nephropathy with Microalbuminuria: A 7-Year Follow-Up Study.

The aim of the study was to examine the relationship between the brain natriuretic peptide (BNP) level and prognosis of diabetic nephropathy. The subjects were 100 Japanese outpatients with type 2 diabetes mellitus with microalbuminuria. Associations between metabolic parameters at baseline, including BNP, and prognosis of diabetic nephropathy (progression of diabetic nephropathy, cardiovascular events, and death) were examined for 7 years. In Cox proportional hazard analysis, HbA1c, albumin-creatinine rati...

Long Non-Coding RNA CASC2 Improves Diabetic Nephropathy by Inhibiting JNK Pathway.

It's known that long non-coding RNA CASC2 overexpression inhibit the JNK pathway in some disease models, while JNK pathway activation exacerbates diabetic nephropathy. Therefore we speculate that long non-coding RNA CASC2 can improve diabetic nephropathy by inhibiting JNK pathway. Thus, our study was carried out to investigate the involvement of CASC2 in diabetic nephropathy. We found that serum level of CASC2 was significantly lower in diabetic nephropathy patients than in normal people, and serum level of...

Diabetic nephropathy: is it always there? Assumptions, weaknesses and pitfalls in the diagnosis.

Diabetic nephropathy is defined as a microvascular complication of the kidneys induced by diabetes mellitus and is characterized by albuminuria and progressive loss of kidney function. However, neither albuminuria nor glomerular filtration rate decline are diabetic nephropathy-specific markers, thus the diagnosis of diabetic nephropathy greatly depends on assumptions. Several factors should be taken into account when urinary albumin levels are assessed before establishing the diagnosis of diabetic nephropat...

Rapamycin Reduces Podocyte Apoptosis and is Involved in Autophagy and mTOR/ P70S6K/4EBP1 Signaling.

The purpose of this study was to investigate the impact of rapamycin (RAP) on autophagy in podocytes and the therapeutic effects of RAP on idiopathic membranous nephropathy (IMN).

Prevention of progression of diabetic nephropathy by the SGLT2 inhibitor ipragliflozin in uninephrectomized type 2 diabetic mice.

Diabetic nephropathy is the leading cause of end-stage renal disease in the world. Although recent development of sodium-glucose cotransporter (SGLT) 2 inhibitors offers a new antidiabetic therapeutic strategy, it remains unclear whether such treatments are beneficial for limiting the progression of type 2 diabetic overt nephropathy. This study examined the effect of the SGLT2 inhibitor ipragliflozin on the progression of nephropathy in uninephrectomized KK/A type 2 diabetic mice, which exhibit not only typ...

ROS-Autophagy pathway mediates monocytes-human umbilical vein endothelial cells adhesion induced by apelin-13.

Apelin is the endogenous ligand of APJ receptor. Both monocytes (MCs) and human umbilical vein endothelial cells (HUVECs) express apelin and APJ, which play important roles in the physiological processes of atherosclerosis. Our previous research indicated that apelin-13 promoted MCs-HUVECs adhesion. Here, we further explore the mechanism responsible for MCs-HUVECs adhesion induced by apelin-13. Apelin-13 promoted reactive oxygen species (ROS) generation and NOX4 expression in HUVECs. Apelin-13 inducedautoph...

Enhanced insulin receptor, but not PI3K, signalling protects podocytes from ER stress.

Disruption of the insulin-PI3K-Akt signalling pathway in kidney podocytes causes endoplasmic reticulum (ER) stress, leading to podocyte apoptosis and proteinuria in diabetic nephropathy. We hypothesised that by improving insulin sensitivity we could protect podocytes from ER stress. Here we use established activating transcription factor 6 (ATF6)- and ER stress element (ERSE)-luciferase assays alongside a novel high throughput imaging-based C/EBP homologous protein (CHOP) assay to examine three models of im...

Urinary afamin levels are associated with the progression of diabetic nephropathy.

In this study, we applied quantitative proteomic analysis to identify urinary proteins associated with diabetic nephropathy (DN).

Potential Value of Urinary Exosome-Derived let-7c-5p in the Diagnosis and Progression of Type II Diabetic Nephropathy.

Diabetic nephropathy (DN) is a leading cause of death worldwide. Reliable biomarkers are demanded for the non-invasive diagnosis of DN. This study aims to investigate whether miRNA in urinary exosomes could serve as a potential biomarker in the diagnosis and progression of DN.

TRPC6-Mediated Ca2+ Signaling is Required for Hypoxia-Induced Autophagy in Human Podocytes.

Intracellular Ca2+ signaling plays an important role in the regulation of autophagy. However, very little is known about the role of Ca2+ influx, which is induced by plasma membrane Ca2+ channels. Our previous study showed that transient receptor potential canonical channel-6 (TRPC6), a major Ca2+ influx pathway in podocytes, was activated by hypoxia. Here, we investigated whether TRPC6 is involved in hypoxia-induced autophagy in cultured human podocytes.

Knockdown of NUP160 inhibits cell proliferation, induces apoptosis, autophagy and cell migration, and alters the expression and localization of podocyte associated molecules in mouse podocytes.

Genetic mutations in dozens of monogenic genes can lead to serious podocyte dysfunction, which is a major cause of steroid-resistant nephrotic syndrome (SRNS). The NUP160 gene is expressed in both human kidney and mouse kidney. However, whether knockdown of NUP160 impairs podocytes has not yet been established. Therefore, we knocked down NUP160 by targeted short hairpin RNA (shRNA) in conditionally immortalized mouse podocytes and observed the effect of NUP160 knockdown on the proliferation, apoptosis, auto...

Diabetic dyslipidemia and microvascular complications of diabetes.

Diabetic dyslipidemia is one of the main risk factors for atherosclerosis. Although its participation in diabetic microvascular complications is not that dominant, dyslipidemia may play an important role in formation and progression of these complications. Pathophysiological mechanisms by which diabetic dyslipidemia affects the etiopathogenesis of diabetic nephropathy, retinopathy, neuropathy and diabetic foot are presented. The data from clinical studies and treatment possibilities for particular microvasc...

Antidiabetic and renoprotective effect of Anogeissus acuminata leaf extract on experimentally induced diabetic nephropathy.

Diabetic nephropathy is the leading cause of end-stage renal disease. Hyperglycemia, oxidative stress, and inflammation are some of the mechanisms involved in renal damage. Anogeissus acuminata (AA) is used in India as an antidiabetic agent and has potent antioxidant activity. However, it has never been evaluated for its effect on diabetic nephropathy. Hence, in the present study we aimed to evaluate its effect on streptozotocin-induced diabetes mellitus and its renal complications.

AGE-RAGE axis blockade in diabetic nephropathy: current status and future directions.

Diabetic nephropathy is one of the most frequent micro-vascular complications both in type 1 and type 2 diabetic patients and is the leading cause of end-stage renal disease worldwide. Although disparate mechanisms give rise to the development of diabetic nephropathy, prevailing evidence accentuates that hyperglycemia-associated generation of advanced glycation end products (AGEs) plays a central role in the disease pathophysiology. Engagement of the receptor for AGE (RAGE) with its ligands provokes oxidati...

Effects of exercise training on adipose tissue apelin expression in streptozotocin-nicotinamide induced diabetic rats.

Apelin is an adipocyte-derived peptide that plays an important role in regulation of energy homoeostasis and decrease of insulin resistance. We investigated the effects of exercise training on adipose tissue apelin expression in streptozotocin-nicotinamide induced diabetic rats. In this experimental study, 38 male Wistar rats were assigned to 4 groups: sedentary diabetic, trained diabetic, sedentary non-diabetic and trained non-diabetic. Type 2 diabetes mellitus (T2DM) was induced by intraperitoneal injecti...

Metformin attenuates diabetes-induced tau hyperphosphorylation in vitro and in vivo by enhancing autophagic clearance.

Diabetes mellitus (DM) can increase the risk of Alzheimer's disease (AD) in patients. However, no effective approaches are available to prevent its progression and development. Recently, autophagy dysfunction was identified to be involved in the pathogenesis of neurodegenerative diseases. This study was designed to investigate the effect of metformin on hyperphosphorylated tau proteins in diabetic encephalopathy (DE) by regulating autophagy clearance. db/db mice were randomly divided into four groups, db/+ ...

Effect of post-transplant glycemic control on long-term clinical outcomes in kidney transplant recipients with diabetic nephropathy: A multicenter cohort study in Korea.

Diabetic nephropathy is the leading cause of end stage renal disease. The number of kidney transplantation (KT) due to diabetic nephropathy is increasing and there is debate on glycemic control after KT. In this study, we used a multi-center database to determine the relationship between post-transplant glycemic control and the outcomes of KT in patients with diabetic nephropathy.

Lectin-induced renal local complement activation is involved in tubular interstitial injury in diabetic nephropathy.

Complement has been suggested to be involved in diabetic nephropathy (DN), but the exact significance and underlying mechanisms remain unclear. Data about renal local complement activation in DN patients is scarce. The purpose of the study was to clarify the significance and mechanism of renal local complement activation in DN.

Melatonin Attenuates Endothelial-to-Mesenchymal Transition of Glomerular Endothelial Cells via Regulating miR-497/ROCK in Diabetic Nephropathy.

Endothelial-to-mesenchymal transition (EndMT) of glomerular endothelial cells (GEnCs) can induce albuminuria in diabetic nephropathy. Melatonin attenuates diabetic nephropathy, but its role and mechanism in EndMT of GEnCs in diabetic nephropathy remain unknown.

Angiopoietin-2, Renal Deterioration, Major Adverse Cardiovascular Events and All-Cause Mortality in Patients with Diabetic Nephropathy.

Diabetic nephropathy is the leading cause of end-stage renal disease and accounts for 30∼40% of patients requiring maintenance dialysis, thereby increasing the burden on health insurance programs. Diabetic nephropathy is also the strongest predictor of cardiovascular morbidity and mortality. The aim of this study was to examine whether angiopoietin-2 (Angpt2), a modulator of endothelial function, affects the clinical outcomes of diabetic patients.


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