scholarly journals The Role of Altered Mitochondrial Metabolism in Thyroid Cancer Development and Mitochondria-Targeted Thyroid Cancer Treatment

2021 ◽  
Vol 23 (1) ◽  
pp. 460
Author(s):  
Siarhei A. Dabravolski ◽  
Nikita G. Nikiforov ◽  
Alexander D. Zhuravlev ◽  
Nikolay A. Orekhov ◽  
Liudmila M. Mikhaleva ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Energy Production ◽  
Recent Progress ◽  
Molecular Mechanisms ◽  
Reactive Oxygen Species Generation ◽  
Common Type ◽  
Mitochondrial Metabolism ◽  
Oxygen Species ◽  
Tumour Formation

Thyroid cancer (TC) is the most common type of endocrine malignancy. Tumour formation, progression, and metastasis greatly depend on the efficacy of mitochondria—primarily, the regulation of mitochondria-mediated apoptosis, Ca2+ homeostasis, dynamics, energy production, and associated reactive oxygen species generation. Recent studies have successfully confirmed the mitochondrial aetiology of thyroid carcinogenesis. In this review, we focus on the recent progress in understanding the molecular mechanisms of thyroid cancer relating to altered mitochondrial metabolism. We also discuss the repurposing of known drugs and the induction of mitochondria-mediated apoptosis as a new trend in the development of anti-TC therapy.

scholarly journals The role of mitochondrial bioenergetics and reactive oxygen species in coronary collateral growth

2013 ◽  
Vol 305 (9) ◽  
pp. H1275-H1280 ◽  
Author(s):  
Yuh Fen Pung ◽  
Wai Johnn Sam ◽  
James P. Hardwick ◽  
Liya Yin ◽  
Vahagn Ohanyan ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Synthesis ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Energy Production ◽  
Phenotypic Switching ◽  
Oxygen Species ◽  
Coronary Collateral ◽  
Collateral Growth

Coronary collateral growth is a process involving coordination between growth factors expressed in response to ischemia and mechanical forces. Underlying this response is proliferation of vascular smooth muscle and endothelial cells, resulting in an enlargement in the caliber of arterial-arterial anastomoses, i.e., a collateral vessel, sometimes as much as an order of magnitude. An integral element of this cell proliferation is the process known as phenotypic switching in which cells of a particular phenotype, e.g., contractile vascular smooth muscle, must change their phenotype to proliferate. Phenotypic switching requires that protein synthesis occurs and different kinase signaling pathways become activated, necessitating energy to make the switch. Moreover, kinases, using ATP to phosphorylate their targets, have an energy requirement themselves. Mitochondria play a key role in the energy production that enables phenotypic switching, but under conditions where mitochondrial energy production is constrained, e.g., mitochondrial oxidative stress, this switch is impaired. In addition, we discuss the potential importance of uncoupling proteins as modulators of mitochondrial reactive oxygen species production and bioenergetics, as well as the role of AMP kinase as an energy sensor upstream of mammalian target of rapamycin, the master regulator of protein synthesis.

scholarly journals Metformin Protects H9C2 Cardiomyocytes from High-Glucose and Hypoxia/Reoxygenation Injury via Inhibition of Reactive Oxygen Species Generation and Inflammatory Responses: Role of AMPK and JNK

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Mingyan Hu ◽  
Ping Ye ◽  
Hua Liao ◽  
Manhua Chen ◽  
Feiyan Yang
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Viability ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Compound C ◽  
Hypoxia Reoxygenation

Metformin is a first-line drug for the management of type 2 diabetes. Recent studies suggested cardioprotective effects of metformin against ischemia/reperfusion injury. However, it remains elusive whether metformin provides direct protection against hypoxia/reoxygenation (H/R) injury in cardiomyocytes under normal or hyperglycemic conditions. This study in H9C2 rat cardiomyoblasts was designed to determine cell viability under H/R and high-glucose (HG, 33 mM) conditions and the effects of cotreatment with various concentrations of metformin (0, 1, 5, and 10 mM). We further elucidated molecular mechanisms underlying metformin-induced cytoprotection, especially the possible involvement of AMP-activated protein kinase (AMPK) and Jun NH(2)-terminal kinase (JNK). Results indicated that 5 mM metformin improved cell viability, mitochondrial integrity, and respiratory chain activity under HG and/or H/R (P<0.05). The beneficial effects were associated with reduced levels of reactive oxygen species generation and proinflammatory cytokines (TNF-α, IL-1α, and IL-6) (P<0.05). Metformin enhanced phosphorylation level of AMPK and suppressed HG + H/R induced JNK activation. Inhibitor of AMPK (compound C) or activator of JNK (anisomycin) abolished the cytoprotective effects of metformin. In conclusion, our study demonstrated for the first time that metformin possessed direct cytoprotective effects against HG and H/R injury in cardiac cells via signaling mechanisms involving activation of AMPK and concomitant inhibition of JNK.

scholarly journals Mitochondrial Dysfunction in Obesity and Reproduction

Endocrinology ◽  
2020 ◽  
Vol 162 (1) ◽  
Author(s):  
Manasi Das ◽  
Consuelo Sauceda ◽  
Nicholas J G Webster
Keyword(s):  
Mitochondrial Dysfunction ◽  
Energy Production ◽  
Molecular Mechanisms ◽  
Human Populations ◽  
Metabolic Alterations ◽  
Genetic Manipulations ◽  
The Past ◽  
Calcium Buffering

Abstract Mounting evidence suggests a role for mitochondrial dysfunction in the pathogenesis of many diseases, including type 2 diabetes, aging, and ovarian failure. Because of the central role of mitochondria in energy production, heme biosynthesis, calcium buffering, steroidogenesis, and apoptosis signaling within cells, understanding the molecular mechanisms behind mitochondrial dysregulation and its potential implications in disease is critical. This review will take a journey through the past and summarize what is known about mitochondrial dysfunction in various disorders, focusing on metabolic alterations and reproductive abnormalities. Evidence is presented from studies in different human populations, and rodents with genetic manipulations of pathways known to affect mitochondrial function.

scholarly journals Role of ROS/RNS in Preeclampsia: Are Connexins the Missing Piece?

2020 ◽  
Vol 21 (13) ◽  
pp. 4698 ◽  
Author(s):  
María F. Rozas-Villanueva ◽  
Paola Casanello ◽  
Mauricio A. Retamal
Keyword(s):  
Reactive Nitrogen Species ◽  
Molecular Mechanisms ◽  
Cell Communication ◽  
Transmembrane Proteins ◽  
Pregnancy Complication ◽  
Oxygen Species ◽  
Nitrogen Species ◽  
Gap Junction Channels ◽  
Contraction And Relaxation

Preeclampsia is a pregnancy complication that appears after 20 weeks of gestation and is characterized by hypertension and proteinuria, affecting both mother and offspring. The cellular and molecular mechanisms that cause the development of preeclampsia are poorly understood. An important feature of preeclampsia is an increase in oxygen and nitrogen derived free radicals (reactive oxygen species/reactive nitrogen species (ROS/RNS), which seem to be central players setting the development and progression of preeclampsia. Cell-to-cell communication may be disrupted as well. Connexins (Cxs), a family of transmembrane proteins that form hemichannels and gap junction channels (GJCs), are essential in paracrine and autocrine cell communication, allowing the movement of signaling molecules between cells as well as between the cytoplasm and the extracellular media. GJCs and hemichannels are fundamental for communication between endothelial and smooth muscle cells and, therefore, in the control of vascular contraction and relaxation. In systemic vasculature, the activity of GJCs and hemichannels is modulated by ROS and RNS. Cxs participate in the development of the placenta and are expressed in placental vasculature. However, it is unknown whether Cxs are modulated by ROS/RNS in the placenta, or whether this potential modulation contributes to the pathogenesis of preeclampsia. Our review addresses the possible role of Cxs in preeclampsia, and the plausible modulation of Cxs-formed channels by ROS and RNS. We suggest these factors may contribute to the development of preeclampsia.

The role of mitochondria in axonal degeneration and tissue repair in MS

2012 ◽  
Vol 18 (8) ◽  
pp. 1058-1067 ◽  
Author(s):  
J van Horssen ◽  
ME Witte ◽  
O Ciccarelli
Keyword(s):  
Mitochondrial Dysfunction ◽  
Tissue Repair ◽  
Molecular Mechanisms ◽  
Axonal Degeneration ◽  
Axonal Damage ◽  
Mitochondrial Metabolism ◽  
Imaging Studies ◽  
And Function

Axonal injury is a key feature of multiple sclerosis (MS) pathology and is currently seen as the main correlate for permanent clinical disability. Although little is known about the pathogenetic mechanisms that drive axonal damage and loss, there is accumulating evidence highlighting the central role of mitochondrial dysfunction in axonal degeneration and associated neurodegeneration. The aim of this topical review is to provide a concise overview on the involvement of mitochondrial dysfunction in axonal damage and destruction in MS. Hereto, we will discuss putative pathological mechanisms leading to mitochondrial dysfunction and recent imaging studies performed in vivo in patients with MS. Moreover, we will focus on molecular mechanisms and novel imaging studies that address the role of mitochondrial metabolism in tissue repair. Finally, we will briefly review therapeutic strategies aimed at improving mitochondrial metabolism and function under neuroinflammatory conditions.

scholarly journals Role of Nox4 and Nox2 in Hyperoxia-Induced Reactive Oxygen Species Generation and Migration of Human Lung Endothelial Cells

2009 ◽  
Vol 11 (4) ◽  
pp. 747-764 ◽  
Author(s):  
Srikanth Pendyala ◽  
Irina A Gorshkova ◽  
Peter V. Usatyuk ◽  
Donghong He ◽  
Arjun Pennathur ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Human Lung ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Lung Endothelial Cells ◽  
And Migration

Role of metal-induced reactive oxygen species generation in lung responses caused by residual oil fly ash

2003 ◽  
Vol 28 (1) ◽  
pp. 13-18 ◽  
Author(s):  
Anthony B. Lewis ◽  
Michael D. Taylor ◽  
Jenny R. Roberts ◽  
Stephen S. Leonard ◽  
Xianglin Shi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Fly Ash ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Residual Oil ◽  
Residual Oil Fly Ash ◽  
Oil Fly Ash
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