scholarly journals Role of PI3K in the Progression and Regression of Atherosclerosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yunyun Zhao ◽  
Yongjiang Qian ◽  
Zhen Sun ◽  
Xinyi Shen ◽  
Yaoyao Cai ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Immune Disorders ◽  
Regulatory Factor ◽  
Phosphatidylinositol 3 Kinase ◽  
Surface Receptors ◽  
Extracellular Signals ◽  
Intracellular Signaling Pathways ◽  
Pi3k Activity

Phosphatidylinositol 3 kinase (PI3K) is a key molecule in the initiation of signal transduction pathways after the binding of extracellular signals to cell surface receptors. An intracellular kinase, PI3K activates multiple intracellular signaling pathways that affect cell growth, proliferation, migration, secretion, differentiation, transcription and translation. Dysregulation of PI3K activity, and as aberrant PI3K signaling, lead to a broad range of human diseases, such as cancer, immune disorders, diabetes, and cardiovascular diseases. A growing number of studies have shown that PI3K and its signaling pathways play key roles in the pathophysiological process of atherosclerosis. Furthermore, drugs targeting PI3K and its related signaling pathways are promising treatments for atherosclerosis. Therefore, we have reviewed how PI3K, an important regulatory factor, mediates the development of atherosclerosis and how targeting PI3K can be used to prevent and treat atherosclerosis.

scholarly journals Pathological processes and therapeutic advances in radioiodide refractory thyroid cancer

2017 ◽  
Vol 59 (4) ◽  
pp. R141-R154 ◽  
Author(s):  
Marika H Tesselaar ◽  
Johannes W Smit ◽  
James Nagarajah ◽  
Romana T Netea-Maier ◽  
Theo S Plantinga
Keyword(s):  
Thyroid Cancer ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Medullary Thyroid Cancer ◽  
Disease Remission ◽  
Intracellular Signaling Pathways ◽  
Oncogenic Mutations ◽  
Diagnostics And Therapy ◽  
Disease Present

While in most patients with non-medullary thyroid cancer (TC), disease remission is achieved by thyroidectomy and ablation of tumor remnants by radioactive iodide (RAI), a substantial subgroup of patients with metastatic disease present tumor lesions that have acquired RAI resistance as a result of dedifferentiation. Although oncogenic mutations inBRAF,TERTpromoter andTP53are associated with an increased propensity for induction of dedifferentiation, the role of genetic and epigenetic aberrations and their effects on important intracellular signaling pathways is not yet fully elucidated. Also immune, metabolic, stemness and microRNA pathways have emerged as important determinants of TC dedifferentiation and RAI resistance. These signaling pathways have major clinical implications since their targeting could inhibit TC progression and could enable redifferentiation to restore RAI sensitivity. In this review, we discuss the current insights into the pathological processes conferring dedifferentiation and RAI resistance in TC and elaborate on novel advances in diagnostics and therapy to improve the clinical outcome of RAI-refractory TC patients.

scholarly journals Update on the Pathophysiological Role of Intracellular Signaling Pathways in Atherosclerotic Plaques and Ischemic Myocardium

2012 ◽  
Vol 7 (2) ◽  
pp. 104-110 ◽  
Author(s):  
Fabrizio Montecucco ◽  
Vincent Braunersreuther ◽  
Giorgio Luciano Viviani ◽  
Sébastien Lenglet ◽  
François Mach
Keyword(s):  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Ischemic Myocardium ◽  
Atherosclerotic Plaques ◽  
Intracellular Signaling Pathways ◽  
Pathophysiological Role

scholarly journals Fine-tuned regulation of the PGC-1α gene transcription by different intracellular signaling pathways

2011 ◽  
Vol 300 (3) ◽  
pp. E500-E507 ◽  
Author(s):  
Tao Hong ◽  
Jie Ning ◽  
Xuefeng Yang ◽  
Hui-Yu Liu ◽  
Jianmin Han ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
P38 Mapk ◽  
Gene Transcription ◽  
Intracellular Signaling ◽  
Insulin Response ◽  
P38 Map Kinase ◽  
Mapk Phosphorylation ◽  
Response Elements ◽  
Intracellular Signaling Pathways

It has previously been known that transcription of the PGC-1α gene can be either inhibited or stimulated by p38 MAP kinase (p38 MAPK). To determine whether p38 MAPK plays an inhibitory or stimulatory role in PGC-1α gene transcription, we further investigated the role of p38 MAPK in this study. Our results showed that the basal level of p38 MAPK phosphorylation was increased in gastrocnemius of mice under HFD and that p38 MAPK stimulated PGC-1α gene transcription in C2C12 myotubes. Our results also provided new mechanisms in myotubes that the p38 MAPK-induced PGC-1α gene transcription was mediated by CREB. In exploring the role of the Akt-dependent insulin signaling on PGC-1α gene transcription, we found that the basal Akt-dependent signaling was increased in gastrocnemius of mice under HFD. The p38 MAPK-induced PGC-1α gene transcription was prevented by insulin. Insulin suppression of PGC-1α gene transcription was neutralized by overexpression of the constitutively nuclear form of FoxO1. Finally, we located three insulin response elements (IREs) in the PGC-1α promoter, and mutations of these IREs abolish or blunt activity of the PGC-1α promoter. Together, our results show that transcription of the PGC-1α gene is balanced by different intracellular signaling pathways.

scholarly journals Role of α7 nicotinic receptor in the immune system and intracellular signaling pathways

2015 ◽  
Vol 3 ◽  
pp. 373-379 ◽  
Author(s):  
Robert Zdanowski ◽  
Małgorzata Krzyżowska ◽  
Dominika Ujazdowska ◽  
Aneta Lewicka ◽  
Sławomir Lewicki
Keyword(s):  
Immune System ◽  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Nicotinic Receptor ◽  
Intracellular Signaling Pathways

Intracellular Signaling Pathways in Human Eosinophil Activation: Role of a β2 Integrin, αMβ2

1999 ◽  
Vol 120 (1) ◽  
pp. 51-53 ◽  
Author(s):  
Masahiko Kato ◽  
Hirokazu Kimura ◽  
Atsushi Tachibana ◽  
Youichi Motegi ◽  
Kenichi Tokuyama ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Intracellular Signaling ◽  
Human Eosinophil ◽  
Intracellular Signaling Pathways ◽  
Eosinophil Activation
Sign in / Sign up

Export Citation Format

Share Document