We are analyzing https://link.springer.com/article/10.1186/s13045-023-01512-7.

Title:
Reactive oxygen species (ROS) scavenging biomaterials for anti-inflammatory diseases: from mechanism to therapy | Journal of Hematology & Oncology
Description:
Inflammation is a fundamental defensive response to harmful stimuli, but the overactivation of inflammatory responses is associated with most human diseases. Reactive oxygen species (ROS) are a class of chemicals that are generated after the incomplete reduction of molecular oxygen. At moderate levels, ROS function as critical signaling molecules in the modulation of various physiological functions, including inflammatory responses. However, at excessive levels, ROS exert toxic effects and directly oxidize biological macromolecules, such as proteins, nucleic acids and lipids, further exacerbating the development of inflammatory responses and causing various inflammatory diseases. Therefore, designing and manufacturing biomaterials that scavenge ROS has emerged an important approach for restoring ROS homeostasis, limiting inflammatory responses and protecting the host against damage. This review systematically outlines the dynamic balance of ROS production and clearance under physiological conditions. We focus on the mechanisms by which ROS regulate cell signaling proteins and how these cell signaling proteins further affect inflammation. Furthermore, we discuss the use of potential and currently available-biomaterials that scavenge ROS, including agents that were engineered to reduce ROS levels by blocking ROS generation, directly chemically reacting with ROS, or catalytically accelerating ROS clearance, in the treatment of inflammatory diseases. Finally, we evaluate the challenges and prospects for the controlled production and material design of ROS scavenging biomaterials.
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28 years and 1 months (reg. 1997-05-29).

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Keywords {🔍}

ros, pubmed, article, google, scholar, central, inflammation, inflammatory, biomaterials, activation, signaling, scavenging, pathway, diseases, cells, antiinflammatory, nfκb, oxygen, production, nlrp, inflammasome, antioxidant, effects, kinase, including, treatment, addition, reactive, protein, cell, nanoparticles, levels, activity, zhang, oxidative, nps, chen, kim, nrf, enzymes, injury, wound, species, mechanisms, mitochondrial, hydrogel, mapk, stress, liu, sod,

Topics {✒️}

nuclear factor kappa-light-chain-enhancer nuclear factor erythroid 2-related factor 2 cnc sod-loaded γ-pgas/γ-pga hydrogel butyrate-loaded chitosan/hyaluronan nanoparticles germline-encoded pattern-recognition receptors c-terminal leucine-rich repeats ischemia-homing bioengineered nano-scavenger nir-driven polydopamine-based nanoenzymes c-jun n-terminal kinase p38-mitogen-activated protein kinase fructose-po-induced hyperuricemic mice uv-light-induced epidermal inflammation enhancing mlk3-dependent b-raf hepatic ischemia-reperfusion injury reactive-oxygen-species-scavenging nanomaterials nf-κb-inducing kinase mapk 15-deoxyd-d-prostaglandin j2 s-allyl-l-cysteine sulfoxide ameliorates pi3k/akt pathway pro-inflammatory mediators-induced airway ros-mediated nf-κb activation reperfusion-induced cerebral injury chlorophyll-loaded liposomal nanoplatform heparin-based hydrogel incorporated ta-conjugated np hydrogel mitogen-activated protein kinase γ-pgas/γ-pga tannin-titanium oxide multilayer treating ischemia-reperfusion injury nuclear transcription factor-kappa intracellular ethanol-mediated oxidation thermo-sensitive hydrogels loaded cardiac ischemia/reperfusion injury mitogen-activated protein kinases curcumin-loaded plga nanoparticles low-molecular-weight ros scavengers n-{5-[2-methylphenyl-6-chlorobenzoxazole]} acetamides age-related macular degeneration ribosomal-s6-kinases msk janus kinase/signal transducer natural enzyme-based biomaterials lipopolysaccharide-induced cyclooxygenase-2 expression l-2-oxothiazolidine-4-carboxylic acid soft tissue wound-healing endogenous bilirubin-based biomaterials tumor necrosis factor-α microglia-mediated inflammatory injury polymerized polydopamine-based nanoparticles n-terminal pyrin domain post-trauma microenvironment-responsive

Questions {❓}

AKT and cancer–is it all mTOR?

Schema {🗺️}

WebPage:
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         headline:Reactive oxygen species (ROS) scavenging biomaterials for anti-inflammatory diseases: from mechanism to therapy
         description:Inflammation is a fundamental defensive response to harmful stimuli, but the overactivation of inflammatory responses is associated with most human diseases. Reactive oxygen species (ROS) are a class of chemicals that are generated after the incomplete reduction of molecular oxygen. At moderate levels, ROS function as critical signaling molecules in the modulation of various physiological functions, including inflammatory responses. However, at excessive levels, ROS exert toxic effects and directly oxidize biological macromolecules, such as proteins, nucleic acids and lipids, further exacerbating the development of inflammatory responses and causing various inflammatory diseases. Therefore, designing and manufacturing biomaterials that scavenge ROS has emerged an important approach for restoring ROS homeostasis, limiting inflammatory responses and protecting the host against damage. This review systematically outlines the dynamic balance of ROS production and clearance under physiological conditions. We focus on the mechanisms by which ROS regulate cell signaling proteins and how these cell signaling proteins further affect inflammation. Furthermore, we discuss the use of potential and currently available-biomaterials that scavenge ROS, including agents that were engineered to reduce ROS levels by blocking ROS generation, directly chemically reacting with ROS, or catalytically accelerating ROS clearance, in the treatment of inflammatory diseases. Finally, we evaluate the challenges and prospects for the controlled production and material design of ROS scavenging biomaterials.
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         Cancer Research
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      name:State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, China
      name:State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, China
      name:State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, China
      name:State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China School of Stomatology, Sichuan University, Chengdu, China
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