Phloretin attenuates hepatic steatosis via improvement of mitochondrial dysfunction by activating AMPK-dependent signaling pathways

2021 ◽  
Author(s):  
Lin Han ◽  
Yao Zhang ◽  
Jia Li ◽  
Yao Xiao ◽  
Mei Lu ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Signaling Pathways ◽  
Hepatic Steatosis ◽  
Biological Activities ◽  
Malus Prunifolia

Phloretin, a dihydrochalcone, widely exists in the fruits of apple and Malus prunifolia with multiple biological activities. Presently, we studied the function of phloretin on the attenuation of hepatic steatosis...

Melatonin As a Modulator of Degenerative and Regenerative Signaling Pathways in Injured Retinal Ganglion Cells

2019 ◽  
Vol 25 (28) ◽  
pp. 3057-3073 ◽  
Author(s):  
Kobra B. Juybari ◽  
Azam Hosseinzadeh ◽  
Habib Ghaznavi ◽  
Mahboobeh Kamali ◽  
Ahad Sedaghat ◽  
...  
Keyword(s):  
Optic Nerve ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathways ◽  
Retinal Ganglion Cells ◽  
Molecular Mechanisms ◽  
Nitrosative Stress ◽  
Ganglion Cells ◽  
Axon Growth ◽  
Nerve Fibers ◽  
Retinal Ganglion

Optic neuropathies refer to the dysfunction or degeneration of optic nerve fibers caused by any reasons including ischemia, inflammation, trauma, tumor, mitochondrial dysfunction, toxins, nutritional deficiency, inheritance, etc. Post-mitotic CNS neurons, including retinal ganglion cells (RGCs) intrinsically have a limited capacity for axon growth after either trauma or disease, leading to irreversible vision loss. In recent years, an increasing number of laboratory evidence has evaluated optic nerve injuries, focusing on molecular signaling pathways involved in RGC death. Trophic factor deprivation (TFD), inflammation, oxidative stress, mitochondrial dysfunction, glutamate-induced excitotoxicity, ischemia, hypoxia, etc. have been recognized as important molecular mechanisms leading to RGC apoptosis. Understanding these obstacles provides a better view to find out new strategies against retinal cell damage. Melatonin, as a wide-spectrum antioxidant and powerful freeradical scavenger, has the ability to protect RGCs or other cells against a variety of deleterious conditions such as oxidative/nitrosative stress, hypoxia/ischemia, inflammatory processes, and apoptosis. In this review, we primarily highlight the molecular regenerative and degenerative mechanisms involved in RGC survival/death and then summarize the possible protective effects of melatonin in the process of RGC death in some ocular diseases including optic neuropathies. Based on the information provided in this review, melatonin may act as a promising agent to reduce RGC death in various retinal pathologic conditions.

scholarly journals Long noncoding RNAs: fine-tuners hidden in the cancer signaling network

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Shanshan Zhao ◽  
Xue Zhang ◽  
Shuo Chen ◽  
Song Zhang
Keyword(s):  
Signaling Pathways ◽  
Cancer Progression ◽  
Biological Activities ◽  
Noncoding Rnas ◽  
Fine Tuning ◽  
Multiple Perspectives ◽  
Sequencing Technology ◽  
Protein Coding ◽  
Abnormal Signal ◽  
Non Coding Rnas

AbstractWith the development of sequencing technology, a large number of long non-coding RNAs (lncRNAs) have been identified in addition to coding genes. LncRNAs, originally considered as junk RNA, are dysregulated in various types of cancer. Although protein-coding signaling pathways underlie various biological activities, and abnormal signal transduction is a key trigger and indicator for tumorigenesis and cancer progression, lncRNAs are sparking keen interest due to their versatile roles in fine-tuning signaling pathways. We are just beginning to scratch the surface of lncRNAs. Therefore, despite the fact that lncRNAs drive malignant phenotypes from multiple perspectives, in this review, we focus on important signaling pathways modulated by lncRNAs in cancer to demonstrate an up-to-date understanding of this emerging field.

scholarly journals Drug-induced hepatic steatosis in absence of severe mitochondrial dysfunction in HepaRG cells: proof of multiple mechanism-based toxicity

2020 ◽  
Author(s):  
Julien Allard ◽  
Simon Bucher ◽  
Julie Massart ◽  
Pierre-Jean Ferron ◽  
Dounia Le Guillou ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Hepatic Steatosis ◽  
Drug Induced ◽  
Multiple Mechanism ◽  
Heparg Cells

scholarly journals pp60c-src is a positive regulator of growth factor-induced cell scattering in a rat bladder carcinoma cell line.

1995 ◽  
Vol 131 (3) ◽  
pp. 761-773 ◽  
Author(s):  
J M Rodier ◽  
A M Vallés ◽  
M Denoyelle ◽  
J P Thiery ◽  
B Boyer
Keyword(s):  
Growth Factor ◽  
Signaling Pathways ◽  
Cell Line ◽  
Intracellular Signaling ◽  
Carcinoma Cell ◽  
Biological Activities ◽  
Dominant Negative ◽  
Carcinoma Cell Line ◽  
Dominant Negative Mutant ◽  
Cell Scattering

The NBT-II rat carcinoma cell line exhibits two mutually exclusive responses to FGF-1 and EGF, entering mitosis at cell confluency while undergoing an epithelium-to-mesenchyme transition (EMT) when cultured at subconfluency. EMT is characterized by acquisition of cell motility, modifications of cell morphology, and cell dissociation correlating with the loss of desmosomes from cellular cortex. The pleiotropic effects of EGF and FGF-1 on NBT-II cells suggest that multiple signaling pathways may be activated. We demonstrate here that growth factor activation is linked to at least two intracellular signaling pathways. One pathway leading to EMT involves an early and sustained stimulation of pp60c-src kinase activity, which is not observed during the growth factor-induced entry into the cell cycle. Overexpression of normal c-src causes a subpopulation of cells to undergo spontaneous EMT and sensitizes the rest of the population to the scattering activity of EGF and FGF-1 without affecting their mitogenic responsiveness. Addition of cholera toxin, a cAMP-elevating agent, severely perturbs growth factor induction of EMT without altering pp60c-src activation, therefore demonstrating that cAMP blockade takes place downstream or independently of pp60c-src. On the other hand, overexpression of a mutated, constitutively activated form of pp60c-src does not block cell dispersion while strongly inhibiting growth factor-induced entry into cell division. Moreover, stable transfection of a dominant negative mutant of c-src inhibits the scattering response without affecting mitogenesis induced by the growth factors. Altogether, these results suggest a role for pp60c-src in epithelial cell scattering and indicate that pp60c-src might contribute unequally to the two separate biological activities engendered by a single signal.

scholarly journals Signaling pathways in mitochondrial dysfunction and aging

2010 ◽  
Vol 131 (7-8) ◽  
pp. 536-543 ◽  
Author(s):  
Cristina Mammucari ◽  
Rosario Rizzuto
Keyword(s):  
Mitochondrial Dysfunction ◽  
Signaling Pathways

scholarly journals Targeting Autophagy with Natural Compounds in Cancer: A Renewed Perspective from Molecular Mechanisms to Targeted Therapy

2021 ◽  
Vol 12 ◽  
Author(s):  
Qiang Xie ◽  
Yi Chen ◽  
Huidan Tan ◽  
Bo Liu ◽  
Ling-Li Zheng ◽  
...  
Keyword(s):  
Natural Products ◽  
Cancer Therapy ◽  
Signaling Pathways ◽  
Small Molecule ◽  
Molecular Mechanisms ◽  
Biological Activities ◽  
Natural Compounds ◽  
Therapeutic Effects ◽  
Therapeutic Benefits ◽  
Small Molecule Drugs

Natural products are well-characterized to have pharmacological or biological activities that can be of therapeutic benefits for cancer therapy, which also provide an important source of inspiration for discovery of potential novel small-molecule drugs. In the past three decades, accumulating evidence has revealed that natural products can modulate a series of key autophagic signaling pathways and display therapeutic effects in different types of human cancers. In this review, we focus on summarizing some representative natural active compounds, mainly including curcumin, resveratrol, paclitaxel, Bufalin, and Ursolic acid that may ultimately trigger cancer cell death through the regulation of some key autophagic signaling pathways, such as RAS-RAF-MEK-ERK, PI3K-AKT-mTOR, AMPK, ULK1, Beclin-1, Atg5 and p53. Taken together, these inspiring findings would shed light on exploiting more natural compounds as candidate small-molecule drugs, by targeting the crucial pathways of autophagy for the future cancer therapy.

scholarly journals The Stemness of Human Ovarian Granulosa Cells and the Role of Resveratrol in the Differentiation of MSCs—A Review Based on Cellular and Molecular Knowledge

Cells ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 1418 ◽  
Author(s):  
Malgorzata Jozkowiak ◽  
Greg Hutchings ◽  
Maurycy Jankowski ◽  
Katarzyna Kulcenty ◽  
Paul Mozdziak ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Granulosa Cells ◽  
Current Knowledge ◽  
Biological Activities ◽  
Primordial Follicle ◽  
Biochemical Processes ◽  
Ovarian Granulosa Cells ◽  
Physiological Properties

Ovarian Granulosa Cells (GCs) are known to proliferate in the developing follicle and undergo several biochemical processes during folliculogenesis. They represent a multipotent cell population that has been differentiated to neuronal cells, chondrocytes, and osteoblasts in vitro. However, progression and maturation of GCs are accompanied by a reduction in their stemness. In the developing follicle, GCs communicate with the oocyte bidirectionally via gap junctions. Together with neighboring theca cells, they play a crucial role in steroidogenesis, particularly the production of estradiol, as well as progesterone following luteinization. Many signaling pathways are known to be important throughout the follicle development, leading either towards luteinization and release of the oocyte, or follicular atresia and apoptosis. These signaling pathways include cAMP, PI3K, SMAD, Hedgehog (HH), Hippo and Notch, which act together in a complex manner to control the maturation of GCs through regulation of key genes, from the primordial follicle to the luteal phase. Small molecules such as resveratrol, a phytoalexin found in grapes, peanuts and other dietary constituents, may be able to activate/inhibit these signaling pathways and thereby control physiological properties of GCs. This article reviews the current knowledge about granulosa stem cells, the signaling pathways driving their development and maturation, as well as biological activities of resveratrol and its properties as a pro-differentiation agent.

scholarly journals Type I Interferon (IFN)-Regulated Activation of Canonical and Non-Canonical Signaling Pathways

2020 ◽  
Vol 11 ◽  
Author(s):  
Candice Mazewski ◽  
Ricardo E. Perez ◽  
Eleanor N. Fish ◽  
Leonidas C. Platanias
Keyword(s):  
Signaling Pathways ◽  
Transcriptional Activation ◽  
Biological Activities ◽  
Mrna Translation ◽  
Type I Interferons ◽  
Type I ◽  
Stat Proteins ◽  
Recombinant Type ◽  
Canonical Pathways ◽  
Recent Developments

For several decades there has been accumulating evidence implicating type I interferons (IFNs) as key elements of the immune response. Therapeutic approaches incorporating different recombinant type I IFN proteins have been successfully employed to treat a diverse group of diseases with significant and positive outcomes. The biological activities of type I IFNs are consequences of signaling events occurring in the cytoplasm and nucleus of cells. Biochemical events involving JAK/STAT proteins that control transcriptional activation of IFN-stimulated genes (ISGs) were the first to be identified and are referred to as “canonical” signaling. Subsequent identification of JAK/STAT-independent signaling pathways, critical for ISG transcription and/or mRNA translation, are denoted as “non-canonical” or “non-classical” pathways. In this review, we summarize these signaling cascades and discuss recent developments in the field, specifically as they relate to the biological and clinical implications of engagement of both canonical and non-canonical pathways.

RNAi-mediated knockdown of DJ-1 leads to mitochondrial dysfunction via Akt/GSK-3ß and JNK signaling pathways in dopaminergic neuron-like cells

2019 ◽  
Vol 146 ◽  
pp. 228-236 ◽  
Author(s):  
Xiao-Ling Zhang ◽  
Zhen-Zhen Wang ◽  
Qian-Hang Shao ◽  
Zhao Zhang ◽  
Lin Li ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Signaling Pathways ◽  
Dopaminergic Neuron ◽  
Jnk Signaling
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