Cracking the Code of UPS in Stroke

Published on April 7, 2022

In the puzzling world of stroke research, secondary damage factors like inflammation, oxidative stress, and mitochondrial dysfunction play a significant role. Current treatments for these damages prove to be disheartening, leaving scientists hungry for innovative strategies. Enter the ubiquitin proteasome system (UPS), the mastermind behind processing key proteins in our cells. This system is vital for maintaining cellular balance and now holds promise in understanding stroke mechanisms. By exploring how UPS interacts with strokes on a molecular level, researchers pave the way for future breakthroughs in stroke treatment. Dive into the article to uncover the detailed research and potential implications of this fascinating connection!

Stroke’s secondary damage, such as inflammation, oxidative stress, and mitochondrial dysfunction, are thought to be crucial factors in the disease’s progression. Despite the fact that there are numerous treatments for secondary damage following stroke, such as antiplatelet therapy, anticoagulant therapy, surgery, and so on, the results are disappointing and the side effects are numerous. It is critical to develop novel and effective strategies for improving patient prognosis. The ubiquitin proteasome system (UPS) is the hub for the processing and metabolism of a wide range of functional regulatory proteins in cells. It is critical for the maintenance of cell homeostasis. With the advancement of UPS research in recent years, it has been discovered that UPS is engaged in a variety of physiological and pathological processes in the human body. UPS is expected to play a role in the onset and progression of stroke via multiple targets and pathways. This paper explores the method by which UPS participates in the linked pathogenic process following stroke, in order to give a theoretical foundation for further research into UPS and stroke treatment.

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