Nitric oxide involvement in the disability and active disease of multiple sclerosis: Systematic review and meta-analysis

Silva, Brenda da; Viero, Fernanda Tibolla; Rodrigues, Patrícia; Trevisan, Gabriela

doi:10.1016/j.niox.2024.01.006

Nitric Oxide

2024

DOI: 10.1016/j.niox.2024.01.006

|View full text |Cite

Nitric oxide involvement in the disability and active disease of multiple sclerosis: Systematic review and meta-analysis

Brenda da Silva,

Fernanda Tibolla Viero,

Patrícia Rodrigues

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Citation Types

Supporting

Mentioning

Contrasting

Year Published

2024

Publication Types

Select...

Article2

Relationship

Self Cite0

Independent2

Authors

Journals

Cited by 2 publications

(1 citation statement)

References 63 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Normally, the basal level of NO throughout the body is low, mainly due to the activities of neuronal NOS (nNOS) and endothelial NOS (eNOS). In contrast, once triggered, inducible NOS (iNOS) generated on-site high output of NO (up to what concentration is still under debate, the μM level most told) for prolonged periods in a variety of acute and chronic inflammatory diseases such as sepsis, organ transplant rejection, vascular dysfunction in asthma, arthritis, diabetes, inflammatory diseases of the gut, and multiple sclerosis. − NO and NOS are also ubiquitous in malignant tumors, especially in relation to angiogenesis and vascular functions. , …”

mentioning

confidence: 99%

Positron Emission Tomography of Nitric Oxide by a Specific Radical-Generating Dihydropyridine Tracer

Zhang,

Li,

et al. 2024

ACS Sens.

View full text Add to dashboard Cite

Nitric oxide (NO) plays a pivotal role as a biological signaling molecule, presenting challenges in its specific detection and differentiation from other reactive nitrogen and oxygen species within living organisms. Herein, a 18F-labeled (fluorine-18, t 1/2 = 109.7 min) small-molecule tracer dimethyl 4-(4-(4-[18F]fluorobutoxy)benzyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylate ([18F]BDHP) is developed based on the dihydropyridine scaffold for positron emission tomography (PET) imaging of NO in vivo. [18F]BDHP exhibits a highly sensitive and efficient C–C cleavage reaction specifically triggered by NO under physiological conditions, leading to the production of a 18F-labeled radical that is readily retained within the cells. High uptakes of [18F]BDHP are found within and around NO-generating cells, such as macrophages treated with lipopolysaccharide or benzo(a)pyrene. MicroPET/CT imaging of arthritic animal model mice reveals distinct tracer accumulation in the arthritic legs, showcasing a higher distribution of NO compared with the control legs. In summary, a specific radical-generating dihydropyridine tracer with a unique radical retention strategy has been established for the marking of NO in real-time in vivo.

show abstract

mentioning

confidence: 99%

Positron Emission Tomography of Nitric Oxide by a Specific Radical-Generating Dihydropyridine Tracer

Zhang,

Li,

et al. 2024

ACS Sens.

View full text Add to dashboard Cite

show abstract

Orchestrating Stress Responses in Multiple Sclerosis: A Role for Astrocytic IFNγ Signaling

Habean,

Kaiser,

Williams

2024

IJMS

View full text Add to dashboard Cite

Multiple sclerosis (MS) is an inflammatory and neurodegenerative disease that is characterized by the infiltration of peripheral immune cells into the central nervous system (CNS), secretion of inflammatory factors, demyelination, and axonal degeneration. Inflammatory mediators such as cytokines alter cellular function and activate resident CNS cells, including astrocytes. Notably, interferon (IFN)γ is a prominent pleiotropic cytokine involved in MS that contributes to disease pathogenesis. Astrocytes are dynamic cells that respond to changes in the cellular microenvironment and are highly responsive to many cytokines, including IFNγ. Throughout the course of MS, intrinsic cell stress is initiated in response to inflammation, which can impact the pathology. It is known that cell stress is pronounced during MS; however, the specific mechanisms relating IFNγ signaling to cell stress responses in astrocytes are still under investigation. This review will highlight the current literature regarding the impact of IFN[gamma symbol] signaling alone and in combination with other immune mediators on astrocyte synthesis of free oxygen radicals and cell death, and cover what is understood regarding astrocytic mitochondrial dysfunction and endoplasmic reticulum stress.

show abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Made with 💙 for researchers

Part of the Research Solutions Family.

Nitric oxide involvement in the disability and active disease of multiple sclerosis: Systematic review and meta-analysis

Cited by 2 publications

References 63 publications

Positron Emission Tomography of Nitric Oxide by a Specific Radical-Generating Dihydropyridine Tracer

Positron Emission Tomography of Nitric Oxide by a Specific Radical-Generating Dihydropyridine Tracer

Orchestrating Stress Responses in Multiple Sclerosis: A Role for Astrocytic IFNγ Signaling

Contact Info

Product

Resources

About