Protective autophagy elicited by RAF→MEK→ERK inhibition suggests a treatment strategy for RAS-driven cancers DOI
Conan G. Kinsey,

Soledad A. Camolotto,

Amélie Boespflug

et al.

Nature Medicine, Journal Year: 2019, Volume and Issue: 25(4), P. 620 - 627

Published: March 4, 2019

Language: Английский

Repertoires of Autophagy in the Pathogenesis of Ocular Diseases DOI Creative Commons
Yujie Li, Qin Jiang,

Guo-Fan Cao

et al.

Cellular Physiology and Biochemistry, Journal Year: 2015, Volume and Issue: 35(5), P. 1663 - 1676

Published: Jan. 1, 2015

Age-related macular degeneration (AMD) is the most common reason of visual impairment in elderly Western countries. The retinal pigment epithelial cells (RPE) causes secondarily adverse effects on neural retina leading to loss. aging characteristics RPE involve lysosomal accumulation lipofuscin and extracellular protein aggregates called "drusen". Molecular mechanisms behind aggregations are weakly understood. There intriguing evidence suggesting that SQSTM1/p62, together with autophagy, has a role pathology different degenerative diseases. It appears SQSTM1/p62 connecting link between autophagy proteasome mediated proteolysis, expressed strongly under exposure various oxidative stimuli proteasomal inhibition. ELAVL1/HuR post-transcriptional factor, which acts mainly as positive regulator gene expression by binding specific mRNAs whose corresponding proteins fundamental for key cellular functions. We here show that, inhibitor MG-132, up-regulated at both mRNA levels, this binds post-transcriptionally regulates ARPE-19 cell line. Furthermore, we observed inhibition caused bound irreversibly perinuclear aggregates. addition AMPK activator AICAR was pro-survival promoted cleansing former complex, but not accumulation, indeed decreased through autophagy-mediated degradation, while pathway. Interestingly, when compared human controls, AMD donor samples strong rather than drusen rich area impaired AMD.

Language: Английский

Citations

16091

AKT/PKB Signaling: Navigating the Network DOI Creative Commons
Brendan D. Manning, Alex Toker

Cell, Journal Year: 2017, Volume and Issue: 169(3), P. 381 - 405

Published: April 1, 2017

Language: Английский

Citations

3027

Mitochondria: In Sickness and in Health DOI Creative Commons
Jodi Nunnari, Anu Suomalainen

Cell, Journal Year: 2012, Volume and Issue: 148(6), P. 1145 - 1159

Published: March 1, 2012

Language: Английский

Citations

2939

Reactive Oxygen Species in Metabolic and Inflammatory Signaling DOI Open Access
Steven J. Forrester, Daniel S. Kikuchi, Marina S. Hernandes

et al.

Circulation Research, Journal Year: 2018, Volume and Issue: 122(6), P. 877 - 902

Published: March 15, 2018

Reactive oxygen species (ROS) are well known for their role in mediating both physiological and pathophysiological signal transduction. Enzymes subcellular compartments that typically produce ROS associated with metabolic regulation, diseases dysfunction may be influenced by changes redox balance. In this review, we summarize the current literature surrounding inflammatory focusing on transduction its relationship to disease progression. particular, examine production such as cytoplasm, mitochondria, peroxisome, endoplasmic reticulum discuss how influence processes proteasome function, autophagy, general signaling. We also highlight of regulation metabolic/inflammatory including atherosclerosis, diabetes mellitus, stroke. order develop therapies target oxidative signaling, it is vital understand balance signaling plays physiology pathophysiology, manipulation identity cellular tissue homeostasis. An increased understanding specific sources an appreciation metabolism help guide us effort treat cardiovascular diseases.

Language: Английский

Citations

1619

Ageing as a Risk Factor for Disease DOI Creative Commons
Teresa Niccoli, Linda Partridge

Current Biology, Journal Year: 2012, Volume and Issue: 22(17), P. R741 - R752

Published: Sept. 1, 2012

Language: Английский

Citations

1550

Mechanisms of physiological and pathological cardiac hypertrophy DOI
Michinari Nakamura, Junichi Sadoshima

Nature Reviews Cardiology, Journal Year: 2018, Volume and Issue: 15(7), P. 387 - 407

Published: April 19, 2018

Language: Английский

Citations

1267

Cancer metabolism: fatty acid oxidation in the limelight DOI
Arkaitz Carracedo, Lewis C. Cantley, Pier Paolo Pandolfi

et al.

Nature reviews. Cancer, Journal Year: 2013, Volume and Issue: 13(4), P. 227 - 232

Published: Feb. 28, 2013

Language: Английский

Citations

1150

The Role of Estrogens in Control of Energy Balance and Glucose Homeostasis DOI Open Access
Franck Mauvais‐Jarvis, Deborah J. Clegg, Andrea L. Hevener

et al.

Endocrine Reviews, Journal Year: 2013, Volume and Issue: 34(3), P. 309 - 338

Published: May 30, 2013

Estrogens play a fundamental role in the physiology of reproductive, cardiovascular, skeletal, and central nervous systems. In this report, we review literature both rodents humans on estrogens their receptors control energy homeostasis glucose metabolism health metabolic diseases. Estrogen actions hypothalamic nuclei differentially food intake, expenditure, white adipose tissue distribution. skeletal muscle, liver, tissue, immune cells are involved insulin sensitivity as well prevention lipid accumulation inflammation. pancreatic islet β-cells also regulate secretion, nutrient homeostasis, survival. deficiency promotes dysfunction predisposing to obesity, syndrome, type 2 diabetes. We discuss effect selective estrogen receptor modulators disorders.

Language: Английский

Citations

1111

Autophagy in malignant transformation and cancer progression DOI
Lorenzo Galluzzi, Federico Pietrocola, José Manuel Bravo‐San Pedro

et al.

The EMBO Journal, Journal Year: 2015, Volume and Issue: 34(7), P. 856 - 880

Published: Feb. 23, 2015

Language: Английский

Citations

1089

Mitochondrial energetics in the kidney DOI

Pallavi Bhargava,

Rick G. Schnellmann

Nature Reviews Nephrology, Journal Year: 2017, Volume and Issue: 13(10), P. 629 - 646

Published: Aug. 14, 2017

Language: Английский

Citations

1004