Please use this identifier to cite or link to this item: https://hdl.handle.net/10316/113179
DC FieldValueLanguage
dc.contributor.authorSohrab, Sayed Sartaj-
dc.contributor.authorRaj, Riya-
dc.contributor.authorNagar, Amka-
dc.contributor.authorHawthorne, Susan-
dc.contributor.authorPaiva-Santos, Ana Cláudia-
dc.contributor.authorKamal, Mohammad Amjad-
dc.contributor.authorEl-Daly, Mai M.-
dc.contributor.authorAzhar, Esam I.-
dc.contributor.authorSharma, Ankur-
dc.date.accessioned2024-02-08T09:34:47Z-
dc.date.available2024-02-08T09:34:47Z-
dc.date.issued2023-05-29-
dc.identifier.issn1420-3049pt
dc.identifier.urihttps://hdl.handle.net/10316/113179-
dc.description.abstractThe body's normal immune response against any invading pathogen that causes infection in the body results in inflammation. The sudden transformation in inflammation leads to the rise of inflammatory diseases such as chronic inflammatory bowel disease, autoimmune disorders, and colorectal cancer (different types of cancer develop at the site of chronic infection and inflammation). Inflammation results in two ways: short-term inflammation i.e., non-specific, involves the action of various immune cells; the other results in long-term reactions lasting for months or years. It is specific and causes angiogenesis, fibrosis, tissue destruction, and cancer progression at the site of inflammation. Cancer progression relies on the interaction between the host microenvironment and tumor cells along with the inflammatory responses, fibroblast, and vascular cells. The two pathways that have been identified connecting inflammation and cancer are the extrinsic and intrinsic pathways. Both have their own specific role in linking inflammation to cancer, involving various transcription factors such as Nuclear factor kappa B, Activator of transcription, Single transducer, and Hypoxia-inducible factor, which in turn regulates the inflammatory responses via Soluble mediators cytokines (such as Interleukin-6, Hematopoietin-1/Erythropoietin, and tumor necrosis factor), chemokines (such as Cyclooxygenase-2, C-X-C Motif chemokines ligand-8, and IL-8), inflammatory cells, cellular components (such as suppressor cells derived from myeloid, tumor-associated macrophage, and acidophils), and promotes tumorigenesis. The treatment of these chronic inflammatory diseases is challenging and needs early detection and diagnosis. Nanotechnology is a booming field nowadays for its rapid action and easy penetration inside the infected destined cells. Nanoparticles are widely classified into different categories based on their different factors and properties such as size, shape, cytotoxicity, and others. Nanoparticles emerged as excellent with highly progressive medical inventions to cure diseases such as cancer, inflammatory diseases, and others. Nanoparticles have shown higher binding capacity with the biomolecules in inflammation reduction and lowers the oxidative stress inside tissue/cells. In this review, we have overall discussed inflammatory pathways that link inflammation to cancer, major inflammatory diseases, and the potent action of nanoparticles in chronic inflammation-related diseases.pt
dc.language.isoengpt
dc.publisherMDPIpt
dc.relationInstitutional Fund Projects under grant No. (IFPIP:513- 141-1443)pt
dc.relationministry of Education and King Abdulaziz University, DSR, Jeddah, Saudi: IFPIP:513-141-1443pt
dc.rightsopenAccesspt
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt
dc.subjectcancerpt
dc.subjectinflammationpt
dc.subjectnanoparticlespt
dc.subjectdrug deliverypt
dc.subjectinflammatory pathwayspt
dc.subject.meshHumanspt
dc.subject.meshCytokinespt
dc.subject.meshNF-kappa Bpt
dc.subject.meshChemokinespt
dc.subject.meshTumor Microenvironmentpt
dc.subject.meshInflammationpt
dc.subject.meshNeoplasmspt
dc.titleChronic Inflammation's Transformation to Cancer: A Nanotherapeutic Paradigmpt
dc.typearticle-
degois.publication.firstPage4413pt
degois.publication.issue11pt
degois.publication.titleMoleculespt
dc.peerreviewedyespt
dc.identifier.doi10.3390/molecules28114413pt
degois.publication.volume28pt
dc.date.embargo2023-05-29*
uc.date.periodoEmbargo0pt
item.fulltextCom Texto completo-
item.grantfulltextopen-
item.languageiso639-1en-
item.cerifentitytypePublications-
item.openairetypearticle-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
crisitem.author.orcid0000-0003-2710-6000-
Appears in Collections:FFUC- Artigos em Revistas Internacionais
Files in This Item:
Show simple item record

Google ScholarTM

Check

Altmetric

Altmetric


This item is licensed under a Creative Commons License Creative Commons