scholarly journals Research Progress on Mechanism of Podocyte Depletion in Diabetic Nephropathy

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Haoran Dai ◽  
Qingquan Liu ◽  
Baoli Liu
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathways ◽  
Rho Gtpases ◽  
Mammalian Target Of Rapamycin ◽  
Adenosine Monophosphate ◽  
Research Progress ◽  
Diabetic Microangiopathy ◽  
Morphological Alterations ◽  
Initial Stage ◽  
Podocyte Detachment

Diabetic nephropathy (DN) together with glomerular hyperfiltration has been implicated in the development of diabetic microangiopathy in the initial stage of diabetic diseases. Increased amounts of urinary protein in DN may be associated with functional and morphological alterations of podocyte, mainly including podocyte hypertrophy, epithelial-mesenchymal transdifferentiation (EMT), podocyte detachment, and podocyte apoptosis. Accumulating studies have revealed that disruption in multiple renal signaling pathways had been critical in the progression of these pathological damages, such as adenosine monophosphate-activated kinase signaling pathways (AMPK), wnt/β-catenin signaling pathways, endoplasmic reticulum stress-related signaling pathways, mammalian target of rapamycin (mTOR)/autophagy pathway, and Rho GTPases. In this review, we highlight new molecular insights underlying podocyte injury in the progression of DN, which offer new therapeutic targets to develop important renoprotective treatments for DN over the next decade.

scholarly journals Research Progress on the Pathological Mechanisms of Podocytes in Diabetic Nephropathy

2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Lili Zhang ◽  
Zhige Wen ◽  
Lin Han ◽  
Yujiao Zheng ◽  
Yu Wei ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Morphological Changes ◽  
Research Progress ◽  
Podocyte Injury ◽  
Functional Changes ◽  
Pathological Mechanism ◽  
Podocyte Detachment ◽  
Stage Renal Disease ◽  
End Stage ◽  
Multiple Signaling

Diabetic nephropathy (DN) is not only an important microvascular complication of diabetes but also the main cause of end-stage renal disease. Studies have shown that the occurrence and development of DN are closely related to morphological and functional changes in podocytes. A series of morphological changes after podocyte injury in DN mainly include podocyte hypertrophy, podocyte epithelial-mesenchymal transdifferentiation, podocyte detachment, and podocyte apoptosis; functional changes mainly involve podocyte autophagy. More and more studies have shown that multiple signaling pathways play important roles in the progression of podocyte injury in DN. Here, we review research progress on the pathological mechanism of morphological and functional changes in podocytes associated with DN, to provide a new target for delaying the occurrence and development of this disorder.

The Involvement of the Mammalian Target of Rapamycin, Protein Tyrosine Phosphatase 1b and Dipeptidase 4 Signaling Pathways in Cancer and Diabetes: A Narrative Review

2020 ◽  
Vol 20 ◽  
Author(s):  
Jiajia Zhang ◽  
Ning Wu ◽  
Dayong Shi
Keyword(s):  
Signaling Pathways ◽  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Mammalian Target Of Rapamycin ◽  
Eukaryotic Cell ◽  
Target Of Rapamycin ◽  
Protein Tyrosine Phosphatase 1B ◽  
Protein Tyrosine ◽  
Transduction Mechanisms ◽  
Specific Proteins

Background: The mammalian target of rapamycin (mTOR), protein tyrosine phosphatase 1b (PTP1B) and dipeptidase 4 (DPP4) signaling pathways regulate eukaryotic cell proliferation and metabolism. Previous researches described different transduction mechanisms in the progression of cancer and diabetes. Methodology: We reviewed recent advances in the signal transduction pathways of mTOR, PTP1B and DPP4 regulation and determined the crosstalk and common pathway in diabetes and cancer. Results: We showed that according to numerous past studies, the proteins participate in the signaling networks for both diseases. Conclusion: There are common pathways and specific proteins involved in diabetes and cancer. This article demonstrates and explains the potential mechanisms of association and future prospects for targeting these proteins in pharmacological studies.

scholarly journals Signaling Mechanisms in the Regulation of Renal Matrix Metabolism in Diabetes

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Meenalakshmi M. Mariappan
Keyword(s):  
Extracellular Matrix ◽  
Signaling Pathways ◽  
Matrix Protein ◽  
Structural Changes ◽  
Mammalian Target Of Rapamycin ◽  
Adverse Outcomes ◽  
Matrix Proteins ◽  
Extracellular Matrix Protein ◽  
Renal Hypertrophy ◽  
Matrix Metabolism

Renal hypertrophy and accumulation of extracellular matrix proteins are among cardinal manifestations of diabetic nephropathy. TGF beta system has been implicated in the pathogenesis of these manifestations. Among signaling pathways activated in the kidney in diabetes, mTOR- (mammalian target of rapamycin-)regulated pathways are pivotal in orchestrating high glucose-induced production of ECM proteins leading to functional and structural changes in the kidney culminating in adverse outcomes. Understanding signaling pathways that influence individual matrix protein expression could lead to the development of new interventional strategies. This paper will highlight some of the diverse components of the signaling network stimulated by hyperglycemia with an emphasis on extracellular matrix protein metabolism in the kidney in diabetes.

Mechanical signal transduction in skeletal muscle growth and adaptation

2005 ◽  
Vol 98 (5) ◽  
pp. 1900-1908 ◽  
Author(s):  
James G. Tidball
Keyword(s):  
Skeletal Muscle ◽  
Signal Transduction ◽  
Mechanical Activation ◽  
Signaling Pathways ◽  
Mechanical Stimulation ◽  
Muscle Growth ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Mechanical Signal ◽  
Igf I

The adaptability of skeletal muscle to changes in the mechanical environment has been well characterized at the tissue and system levels, but the mechanisms through which mechanical signals are transduced to chemical signals that influence muscle growth and metabolism remain largely unidentified. However, several findings have suggested that mechanical signal transduction in muscle may occur through signaling pathways that are shared with insulin-like growth factor (IGF)-I. The involvement of IGF-I-mediated signaling for mechanical signal transduction in muscle was originally suggested by the observations that muscle releases IGF-I on mechanical stimulation, that IGF-I is a potent agent for promoting muscle growth and affecting phenotype, and that IGF-I can function as an autocrine hormone in muscle. Accumulating evidence shows that at least two signaling pathways downstream of IGF-I binding can influence muscle growth and adaptation. Signaling via the calcineurin/nuclear factor of activated T-cell pathway has been shown to have a powerful influence on promoting the slow/type I phenotype in muscle but can also increase muscle mass. Neural stimulation of muscle can activate this pathway, although whether neural activation of the pathway can occur independent of mechanical activation or independent of IGF-I-mediated signaling remains to be explored. Signaling via the Akt/mammalian target of rapamycin pathway can also increase muscle growth, and recent findings show that activation of this pathway can occur as a response to mechanical stimulation applied directly to muscle cells, independent of signals derived from other cells. In addition, mechanical activation of mammalian target of rapamycin, Akt, and other downstream signals is apparently independent of autocrine factors, which suggests that activation of the mechanical pathway occurs independent of muscle-mediated IGF-I release.

scholarly journals AMP-Activated Protein Kinase as a Key Trigger for the Disuse-Induced Skeletal Muscle Remodeling

2018 ◽  
Vol 19 (11) ◽  
pp. 3558 ◽  
Author(s):  
Natalia Vilchinskaya ◽  
Igor Krivoi ◽  
Boris Shenkman
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Histone Deacetylases ◽  
Molecular Mechanisms ◽  
Weight Bearing ◽  
Mammalian Target Of Rapamycin ◽  
Adenosine Monophosphate ◽  
Chain Gene ◽  
Mtorc1 Signaling ◽  
The Impact

Molecular mechanisms that trigger disuse-induced postural muscle atrophy as well as myosin phenotype transformations are poorly studied. This review will summarize the impact of 5′ adenosine monophosphate -activated protein kinase (AMPK) activity on mammalian target of rapamycin complex 1 (mTORC1)-signaling, nuclear-cytoplasmic traffic of class IIa histone deacetylases (HDAC), and myosin heavy chain gene expression in mammalian postural muscles (mainly, soleus muscle) under disuse conditions, i.e., withdrawal of weight-bearing from ankle extensors. Based on the current literature and the authors’ own experimental data, the present review points out that AMPK plays a key role in the regulation of signaling pathways that determine metabolic, structural, and functional alternations in skeletal muscle fibers under disuse.

scholarly journals Crosstalk Between Autophagy and the cGAS–STING Signaling Pathway in Type I Interferon Production

2021 ◽  
Vol 9 ◽  
Author(s):  
Kunli Zhang ◽  
Sutian Wang ◽  
Hongchao Gou ◽  
Jianfeng Zhang ◽  
Chunling Li
Keyword(s):  
Signaling Pathway ◽  
Adenosine Monophosphate ◽  
Degradation Process ◽  
Guanosine Monophosphate ◽  
Type I Interferons ◽  
Research Progress ◽  
Type I ◽  
Type I Ifn ◽  
Major Pathway ◽  
Sting Pathway

Innate immunity is the front-line defense against infectious microorganisms, including viruses and bacteria. Type I interferons are pleiotropic cytokines that perform antiviral, antiproliferative, and immunomodulatory functions in cells. The cGAS–STING pathway, comprising the main DNA sensor cyclic guanosine monophosphate/adenosine monophosphate synthase (cGAS) and stimulator of IFN genes (STING), is a major pathway that mediates immune reactions and is involved in the strong induction of type I IFN production, which can fight against microbial infections. Autophagy is an evolutionarily conserved degradation process that is required to maintain host health and facilitate capture and elimination of invading pathogens by the immune system. Mounting evidence indicates that autophagy plays an important role in cGAS–STING signaling pathway-mediated type I IFN production. This review briefly summarizes the research progress on how autophagy regulates the cGAS–STING pathway, regulating type I IFN production, with a particular focus on the crosstalk between autophagy and cGAS–STING signaling during infection by pathogenic microorganisms.

scholarly journals Temsirolimus in the treatment of renal cell carcinoma associated with Xp11.2 translocation/TFE gene fusion proteins: a case report and review of literature

Rare Tumors ◽  
2009 ◽  
Vol 1 (2) ◽  
pp. 164-166
Author(s):  
Jigarkumar Parikh ◽  
Teresa Coleman ◽  
Nidia Messias ◽  
James Brown
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathways ◽  
Renal Cell ◽  
Gene Fusion ◽  
Mammalian Target Of Rapamycin ◽  
World Health ◽  
Target Of Rapamycin ◽  
Tyrosine Kinase Receptor ◽  
Xp11.2 Translocation

Xp11.2 translocation renal cell carcinomas (TRCCs) are a rare family of tumors newly recognized by the World Health Organization (WHO) in 2004. These tumors result in the fusion of partner genes to the TFE3 gene located on Xp11.2. They are most common in the pediatric population, but have been recently implicated in adult renal cell carcinoma (RCC) presenting at an early age. TFE3-mediated direct transcriptional upregulation of the Met tyrosine kinase receptor triggers dramatic activation of downstream signaling pathways including the protein kinase B (Akt)/phosphatidylinositol-3 kinase (PI3K) and mammalian target of rapamycin (mTOR) pathways. Temsirolimus is an inhibitor of mammalian target of rapamycin (mTOR) kinase, a component of intracellular signaling pathways involved in the growth and proliferation of malignant cells. Here we present a case of a 22-year old female who has been treated with temsirolimus for her Xp11.2/ TFE3 gene fusion RCC.

scholarly journals Research Progress on the Relationship between Atherosclerosis and Inflammation

Biomolecules ◽  
2018 ◽  
Vol 8 (3) ◽  
pp. 80 ◽  
Author(s):  
Yuhua Zhu ◽  
Xuemei Xian ◽  
Zhenzhen Wang ◽  
Yingchao Bi ◽  
Quangang Chen ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Plaque Rupture ◽  
Chronic Inflammatory Disease ◽  
Research Progress ◽  
Bioactive Lipids ◽  
Inflammatory Signaling ◽  
Vascular Stenosis ◽  
Unstable Atherosclerotic Plaque ◽  
Atherosclerotic Plaque Rupture

Atherosclerosis is a chronic inflammatory disease; unstable atherosclerotic plaque rupture, vascular stenosis, or occlusion caused by platelet aggregation and thrombosis lead to acute cardiovascular disease. Atherosclerosis-related inflammation is mediated by proinflammatory cytokines, inflammatory signaling pathways, bioactive lipids, and adhesion molecules. This review discusses the effects of inflammation and the systemic inflammatory signaling pathway on atherosclerosis, the role of related signaling pathways in inflammation, the formation of atherosclerosis plaques, and the prospects of treating atherosclerosis by inhibiting inflammation.

Translational Aspects of the Mammalian Target of Rapamycin Complexes in Diabetic Nephropathy

2021 ◽  
Author(s):  
Alaa Abou Daher ◽  
Sahar Alkhansa ◽  
William S. Azar ◽  
Rim Rafeh ◽  
Hilda E. Ghadieh ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin
Sign in / Sign up

Export Citation Format

Share Document