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Topic Review
Regulation of Angiogenesis by Non-Coding RNAs in Cancer
Non-coding RNAs, including microRNAs, long non-coding RNAs, and circular RNAs, have been identified as crucial regulators of various biological processes through epigenetic regulation, transcriptional regulation, and post-transcriptional regulation. Growing evidence suggests that dysregulation and activation of non-coding RNAs are closely associated with tumor angiogenesis, a process essential for tumor growth and metastasis and a major contributor to cancer-related mortality. Therefore, understanding the molecular mechanisms underlying tumor angiogenesis is of utmost importance. Numerous studies have documented the involvement of different types of non-coding RNAs in the regulation of angiogenesis. 
  • 237
  • 22 Jan 2024
Topic Review
Regulating and Function of miR-424-5p in Cancers
MiR-424-5p has been widely identified as a tumor suppressor gene that functions in many types of human cancer. It is processed from the 5′ end arm of the miR-424 precursor, is located on human chromosome Xq26.3 and is clustered with miR-15/miR-16. MiR-424 is a member of the miR-16 family.
  • 361
  • 20 Apr 2022
Topic Review
Regenerative Potential (RP) of MSCEVs
Mesenchymal stem cell extracellular vesicles (MSCEVs) obtained from MSCs can have numerous therapeutic applications via regeneration of various body tissues. MSCEV action can be potentiated by modifying the mesenchymal stem cells culturing methodology and bioengineering extracellular vesicles (EVs). 
  • 156
  • 11 Sep 2023
Topic Review
Regenaring Axons and Axon-Glia Interactions
Following an injury, axons of both the central nervous system (CNS) and peripheral nervous system (PNS) degenerate through a coordinated and genetically conserved mechanism known as Wallerian degeneration (WD). Unlike central axons, severed peripheral axons have a higher capacity to regenerate and reinnervate their original targets, mainly because of the favorable environment that they inhabit and the presence of different cell types. Even though many aspects of regeneration in peripheral nerves have been studied, there is still a lack of understanding regarding the dynamics of axonal degeneration and regeneration, mostly due to the inherent limitations of most animal models. In this scenario, the use of zebrafish (Danio rerio) larvae combined with time-lapse microscopy currently offers a unique experimental opportunity to monitor the dynamics of the regenerative process in the PNS in vivo.
  • 400
  • 13 Apr 2021
Topic Review
Redox-Regulation of α-Globin in Vascular Physiology
Interest in the structure, function, and evolutionary relations of circulating and intracellular globins dates back more than 60 years to the first determination of the three-dimensional structure of these proteins. Non-erythrocytic globins have been implicated in circulatory control through reactions that couple nitric oxide (NO) signaling with cellular oxygen availability and redox status. Small artery endothelial cells (ECs) express free α-globin, which causes vasoconstriction by degrading NO. This reaction converts reduced (Fe2+) α-globin to the oxidized (Fe3+) form, which is unstable, cytotoxic, and unable to degrade NO. Therefore, (Fe3+) α-globin must be stabilized and recycled to (Fe2+) α-globin to reinitiate the catalytic cycle. The molecular chaperone α-hemoglobin-stabilizing protein (AHSP) binds (Fe3+) α-globin to inhibit its degradation and facilitate its reduction. The mechanisms that reduce (Fe3+) α-globin in ECs are unknown, although endothelial nitric oxide synthase (eNOS) and cytochrome b5 reductase (CyB5R3) with cytochrome b5 type A (CyB5a) can reduce (Fe3+) α-globin in solution.
  • 639
  • 28 Jan 2022
Topic Review
Redox Network in Mammalian Cells and Selenium Compouds
Redox balance is important for the homeostasis of normal cells, but also for the proliferation, progression, and survival of cancer cells. Both oxidative and reductive stress can be harmful to cells. In contrast to oxidative stress, reductive stress and the therapeutic opportunities underlying the mechanisms of reductive stress in cancer, as well as how cancer cells respond to reductive stress, have received little attention and are not as well characterized. Therefore, there is recent interest in understanding how selective induction of reductive stress may influence therapeutic treatment and disease progression in cancer. There is also the question of how cancer cells respond to reductive stress. Selenium compounds have been shown to have chemotherapeutic effects against cancer and their anticancer mechanism is thought to be related to the formation of their metabolites, including hydrogen selenide (H2Se), which is a highly reactive and reducing molecule and possible can generate the reductive stress in cells. The research report on the molecular mechanism of how cells recognize and respond to oxidative and reductive stress and selenium compounds with well documented hydrogen selenide release, as compounds possibly useful in study of redox homeostasis by the selective induction of reductive stress in cells and in vivo, as well as possibly their utility in anti-cancer therapy.
  • 302
  • 26 Jun 2023
Topic Review
Redox Homeostasis in Pancreatic β-Cells
Redox status is a key determinant in the fate of every cell, β-cell in particular.  β-cells are not primarily detoxifying like e.g. hepatocytes or kidney cells and thus do not possess extensive antioxidant defense machinery. However, they show a wide range of redox regulating proteins, such as peroxiredoxins, thioredoxins or thioredoxin reductases, etc., being functionally compartmentalized. These proteins keep fragile redox homeostasis and serve as messengers and amplifiers of redox signaling which is inevitable for proper β-cell function (particularly insulin secretion) and maintenance. Dysbalance in redox homeostasis establishes oxidative stress which accompanies the development of type 2 diabetes.
  • 435
  • 06 May 2021
Topic Review
Redox Homeostasis in Muscular Dystrophies
Reactive oxygen species are (ROS) are signaling molecules moderately and continuously produced by skeletal muscles as a consequence of their contractile activity and high mitochondrial oxygen consumption. The main source of ROS production is located in the cytosol through the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX enzymes), xanthine oxidase (XO), and nitric oxide synthase (NOS), and by the mitochondrial electron transport chain. When ROS exceed the antioxidant buffering capacity of tissues, oxidative stress occurs.
  • 1.1K
  • 15 Jun 2021
Topic Review
Redox Control in ALL
Acute lymphoblastic leukemia (ALL) is a hematological malignancy originating from B- or T-lymphoid progenitor cells. Recent studies have shown that redox dysregulation caused by overproduction of reactive oxygen species (ROS) has an important role in the development and progression of leukemia. The application of pro-oxidant therapy, which targets redox dysregulation, has achieved satisfactory results in alleviating the conditions of and improving the survival rate for patients with ALL. However, drug resistance and side effects are two major challenges that must be addressed in pro-oxidant therapy. Oxidative stress can activate a variety of antioxidant mechanisms to help leukemia cells escape the damage caused by pro-oxidant drugs and develop drug resistance. Hematopoietic stem cells (HSCs) are extremely sensitive to oxidative stress due to their low levels of differentiation, and the use of pro-oxidant drugs inevitably causes damage to HSCs and may even cause severe bone marrow suppression.
  • 324
  • 01 Jun 2021
Topic Review
Redox Chemistry and Ubiquitylation
The ubiquitin-proteasome system (UPS) is a highly regulated mechanism for protein degradation that regulates many biological processes to maintain cellular homeostasis. A protein is targeted for degradation upon ubiquitylation, where the small 8.6 kDa protein, ubiquitin, is covalently attached to the target protein through an isopeptide bond. Ubiquitylation involves the sequential transfer of ubiquitin through a three-enzyme cascade—an ubiquitin-activating enzyme (E1), an ubiquitin-conjugating enzyme (E2), and an ubiquitin ligase (E3).
  • 408
  • 30 Aug 2021
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