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Cancer Metabolism and Redox Homeostasis of Oxidative Phosphorylat
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<!--===========open access journals=================--> </aside> <div class="col-12 col-sm-9 full-text"> <div class="row align-items-center justify-content-between"> <div class="col-12 col-sm-4"> <p class="text-muted mb-0"> Commentry - (2024)Volume 10, Issue 2 </p> </div> <div class="col-12 col-sm-8 text-right custom-column"> <a href="https://www.longdom.org/articles/cancer-metabolism-and-redox-homeostasis-of-oxidative-phosphorylation-in-cancer-metabolism.pdf" title="View PDF" class="btn btn-sm bg-green-600 rounded-50"><i class="fas fa-file-pdf"></i> View PDF</a> <a href="https://www.longdom.org/pdfdownload.php?download=articles/cancer-metabolism-and-redox-homeostasis-of-oxidative-phosphorylation-in-cancer-metabolism.pdf&aid=109649" title="Download PDF" class="btn btn-sm bg-green-600 rounded-50"><i class="fas fa-download"></i> Download PDF</a> </div> </div> <h2 class="font-size-7 mt-2">Cancer Metabolism and Redox Homeostasis of Oxidative Phosphorylation in Cancer Metabolism</h2> <a href='https://www.longdom.org/author/karen-wetherall-71642' title='Karen Wetherall' style='color:#555; border-bottom:1px dotted #CCC;'>Karen Wetherall</a><sup><a href='#Karen_Wetherall'>*</a></sup> <div> </div> <a id="Karen_Wetherall"></a> <strong><sup>*</sup>Correspondence:</strong> Karen Wetherall, Department of Oncology, Juntendo University, Tokyo, Japan, <strong>Email:</strong> <i class='fa fa-envelope' aria-hidden='true' title='wetherkar@tokyo.ac.jp'></i> <p><a href="#ai"><strong>Author info »</strong></a></p> <h4>About the Study</h4> <p>The process of oxidative phosphorylation is fundamental to the synthesis of cellular energy and is deeply ingrained in the metabolism of all aerobic organisms. This fundamental biochemical process occurs within the mitochondria, where electrons extracted from nutrients during cellular respiration cascade through a series of electron transport chain complexes. These complexes, embedded within the inner mitochondrial membrane, generate a proton gradient that drives ATP synthesis <em>via</em> ATP synthase a molecular machine often likened to a cellular turbine.</p> <p>Beyond its role in ATP production, oxidative phosphorylation represents a marvel of biological efficiency and complexity. It not only sustains essential cellular functions but also integrates closely with cellular signaling, redox regulation, and metabolic adaptation. Dysregulation of oxidative phosphorylation underpins numerous human diseases, underscoring its indispensable role in health and disease. Understanding the complex of this process illuminates pathways for therapeutic interventions targeting mitochondrial dysfunction, offering potential methods to address a wide array of metabolic disorders and age-related conditions.</p> <p><strong>Oxidative phosphorylation in <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cancer-26169.html'>cancer</a> metabolism</strong></p> <p>Its undergoes significant alterations that support the rapid proliferation and survival of <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cancer-26169.html'>cancer</a> cells. While normal <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cells-53612.html'>cells</a> primarily rely on oxidative phosphorylation for ATP production, many <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cancer-26169.html'>cancer</a> <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cells-53612.html'>cells</a> exhibit a metabolic shift towards increased glycolysis, known as the Warburg effect, even in the presence of oxygen a phenomenon termed aerobic glycolysis. Despite this preference for glycolysis, <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cancer-26169.html'>cancer</a> <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cells-53612.html'>cells</a> often maintain functional oxidative phosphorylation, which plays important roles in supplying metabolic intermediates, supporting redox balance, and sustaining cellular bioenergetics under varying conditions within the tumor microenvironment.</p> <p>The dysregulation of oxidative phosphorylation in <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cancer-26169.html'>cancer</a> metabolism is complex and varies depending on tumor type and stage. These metabolic adaptations are important for developing targeted therapies that exploit vulnerabilities in <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cancer-26169.html'>cancer</a> cell metabolism while minimizing effects on normal cells, potentially offering new methods for improving <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cancer-26169.html'>cancer</a> treatment strategies.</p> <p><strong>Oxidative phosphorylation and cellular redox homeostasis</strong></p> <p>Oxidative phosphorylation is complex linked to cellular redox homeostasis, maintaining a delicate balance between oxidation and reduction reactions essential for cellular function and survival. As electrons pass through the electron transport chain in mitochondria, they generate a proton gradient that drives ATP synthesis. Simultaneously, this process produces Reactive Oxygen <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/species-5796.html'>Species</a> (ROS) as natural biproducts.</p> <p>Cellular redox <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/homeostasis-25780.html'>homeostasis</a> involves complex antioxidant defense systems that regulate ROS levels to prevent oxidative damage while utilizing ROS as signaling molecules in cellular processes. Oxidative phosphorylation influences redox balance by controlling the production and <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/detoxification-15599.html'>detoxification</a> of ROS, thereby impacting cell signaling, metabolism, and stress response pathways.</p> <p>Disruptions in oxidative phosphorylation can lead to oxidative stress, characterized by an imbalance between ROS production and antioxidant defenses, contributing to cellular damage and various diseases. Understanding the exchange between oxidative phosphorylation and redox <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/homeostasis-25780.html'>homeostasis</a> is need for deciphering disease mechanisms and developing therapeutic strategies aimed at maintaining cellular health and preventing oxidative damage.</p> <p><strong>Impact of <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/oxidative-stress-2345.html'>oxidative stress</a> on mitochondrial electron transport chain</strong></p> <p>The Electron Transport Chain (ETC) within the mitochondria is significantly impacted by oxidative stress, the primary site of cellular energy production and Reactive Oxygen <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/species-5796.html'>Species</a> (ROS) generation. Elevated ROS levels, arising from conditions such as environmental toxins, metabolic imbalance, or inflammatory responses, can damage mitochondrial components necessary for ETC function, including lipids, proteins, and DNA.</p> <p>Such damage disrupts electron flow within the ETC, impairing ATP production and exacerbating ROS production in a harmful cycle. Additionally, ROS-induced modifications to ETC <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/enzymes-9819.html'>enzymes</a> can further compromise their efficiency, leading to cellular dysfunction and contributing to various diseases, including neurodegenerative disorders, cardiovascular diseases, and <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/cancer-3081.html'>cancer.</a> The impact of <a target='_blank' href='https://www.longdom.org/peer-reviewed-journals/oxidative-stress-2345.html'>oxidative stress</a> on the ETC is important for developing strategies to mitigate ROS-induced damage, restore mitochondrial function, and maintain cellular homeostasis. Research into antioxidant therapies and mitochondrial-targeted interventions aims to counteract these effects, offering potential methods for therapeutic development against oxidative stressrelated diseases. <!----------for extracted references-------> <!-------------------------------> <div class="card bg-light mb-3"> <div class="card-body px-3 pb-0"> <h4 class="font-size-4"><a id="ai"></a>Author Info</h4> <a href='https://www.longdom.org/author/karen-wetherall-71642' title='Karen Wetherall' style='color:#555; border-bottom:1px dotted #CCC;'>Karen Wetherall</a><sup><a href='#Karen_Wetherall'>*</a></sup> <div> </div> Department of Oncology, Juntendo University, Tokyo, Japan<br> <div> </div> <p><strong>Citation:</strong> Wetherall K (2024) Cancer Metabolism and Redox Homeostasis of Oxidative Phosphorylation in Cancer Metabolism. Glob J Lif Sci Biol Res. 10:072.</p> <p> <strong>Received: </strong>15-May-2024, Manuscript No. GJLSBR-24-33086; <strong>Editor assigned: </strong>20-May-2024, Pre QC No. GJLSBR-24-33086 (PQ); <strong>Reviewed: </strong>03-Jun-2024, QC No. GJLSBR-24-33086; <strong>Revised: </strong>10-Jun-2024, Manuscript No. GJLSBR-24-33086 (R); <strong>Published:</strong> 17-Jun-2024 , DOI: 10.35248/2456-3102.24.10.072</p> <p><strong>Copyright: </strong>© 2024 Wetherall K. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</p> </div> </div> </div> </div> </div> </section> <footer class="bg-blue-grey-900 py-3"> <div class="container"> <div class="row"> <div class="col-12 col-sm-4"> <h4 class="white font-size-4 fweight-400 border-bottom-1 pb-2">Content Links</h4> <ul class="list-unstyled footer-links font-size-3"> <li><a class="" href="https://www.longdom.org/online-tools.html" title="Click here">Tools</a> </li> <li><a class="" href="https://www.longdom.org/feedback.html" title="Click here">Feedback</a></li> <li><a class="" href="https://www.longdom.org/careers.html" title="Click here">Careers</a></li> <li><a class="" href="https://www.longdom.org/privacy-policy.html" title="Click here">Privacy Policy</a></li> <li><a class="" href="https://www.longdom.org/terms-conditions.html" title="Click here">Terms & Conditions</a></li> <li><a class="" href="https://www.longdom.org/authors-reviewers-editors.html" title="Click here">Authors, Reviewers & Editors</a></li> </ul> </div> <div class="col-12 col-sm-4"> <h4 class="white font-size-4 fweight-400 border-bottom-1 pb-2">Contact Longdom</h4> <p>Longdom Group SA<br> Avenue Roger Vandendriessche,<br> 18, 1150 Brussels, Belgium<br> Phone: +442038085340 <br><strong>Email:</strong> <a href="mailto:info@longdom.org" class="white" title="Click here">info@longdom.org</a></p> </div> <div class="col-12 col-sm-4"> <h4 class="white font-size-4 fweight-400 border-bottom-1 pb-2">Connect</h4> <nav class="nav nav-pills social-icons-footer flex-column a-pl-0"> <a href="https://www.facebook.com/longdompublisher" title="Click here" target="_blank" class="nav-link bg-facebook-hover"><i class="fab fa-facebook-f bg-facebook"></i> Facebook</a> <a href="https://www.linkedin.com/company/longdom-publishing-sl/" title="Click here" target="_blank" class="nav-link bg-linkedin-hover"><i class="fab fa-linkedin-in bg-linkedin"></i> Linkedin</a> <a href="https://twitter.com/LongdomP" title="Click here" target="_blank" class="nav-link bg-twitter-hover"><i class="fab fa-twitter bg-twitter"></i> Twitter</a> <a href="https://www.instagram.com/longdom_publisher/" title="Click here" target="_blank" class="nav-link bg-instagram-hover"><i class="fab fa-instagram bg-instagram"></i> Instagram</a> </nav> </div> </div> <div class="row text-center"> <div class="col"> <p>Copyright © 2025 <a href="https://www.longdom.org/" title="Click here" class="white">Longdom Publishing</a>.</p> </div> </div> </div> </footer> <!--========================== Scroll To Top ============================--> <a href="#0" class="cd-top js-cd-top">Top</a> <!-- Optional JavaScript --> <!-- jQuery first, then Popper.js, then Bootstrap JS --> <script defer src="https://code.jquery.com/jquery-3.3.1.min.js"></script> <script defer src="https://cdnjs.cloudflare.com/ajax/libs/popper.js/1.14.7/umd/popper.min.js"></script> <script defer src="https://stackpath.bootstrapcdn.com/bootstrap/4.3.1/js/bootstrap.min.js"></script> <!--Get the app icon js--> <script> jQuery(function($) { $(window).scroll(function fix_element() { $('#target').css( $(window).scrollTop() > 100 ? 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