FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W4296110422> ?p ?o ?g. }

• W4296110422 abstract "Immune checkpoint inhibitors (ICIs) have significantly changed the oncology clinic in recent years, improving survival expectations in cancer patients. ICI therapy have a broad spectrum of side effects from endocrinopathies to cardiovascular diseases. In this study, pro-inflammatory and pro-fibrotic effects of short-term ICIs therapy in preclinical models were analyzed.Firstly, in a human in vitro model, human cardiomyocytes co-cultured with hPBMC were exposed to ICIs (with CTLA-4 or PD-1 blocking agents, at 200 nM) for 72 h. After treatment, production of DAMPs and 12 cytokines were analyzed in the supernatant through colorimetric and enzymatic assays. C57/Bl6 mice were treated with CTLA-4 or PD-1 blocking agents (15 mg/kg) for 10 days. Before (T0), after three days (T3) and after treatments (T10), ejection fraction, fractional shortening, radial and longitudinal strain were calculated by using bidimensional echocardiography (Vevo 2100, Fujfilm). Fibrosis, necrosis, hypertrophy and vascular NF-kB expression were analyzed through Immunohistochemistry. Myocardial expression of DAMPs (S100- Calgranulin, Fibronectin and Galectine-3), MyD88, NLRP3 and twelve cytokines have been analyzed. Systemic levels of SDF-1, IL-1β, and IL-6 were analyzed before, during and after ICIs therapy.Radial and longitudinal strain were decreased after 10 days of ICIs therapy. Histological analysis of NF-kB expression shows that short-term anti-CTLA-4 or anti-PD-1 treatment increased vascular and myocardial inflammation. No myocardial hypertrophy was seen with the exception of the pembrolizumab group. Myocardial fibrosis and expression of galectin-3, pro-collagen 1-α and MMP-9 were increased after treatment with all ICIs. Both anti-CTLA-4 or anti-PD-1 treatments increased the expression of DAMPs, NLRP3 inflammasome and MyD88 and induced both in vitro and in vivo the secretion of IL-1β, TNF-α and IL-6. Systemic levels of SDF-1, IL-1β and IL-6 were increased during and after treatment with ICIs.Short therapy with PD-1 and CTLA-4 blocking agents increases vascular expression of NF-kB, systemic SDF-1, IL-1β, IL-6 levels and myocardial NLRP3, MyD88 and DAMPs expression in preclinical models. A pro-inflammatory cytokine storm was induced in myocardial tissues and in cultured cardiac cells after ICIs therapy. The overall picture of the study suggests new putative biomarkers of ICIs-mediated systemic and myocardial damages potentially useful in clinical cardioncology." @default.
• W4296110422 created "2022-09-17" @default.
• W4296110422 creator A5005784207 @default.
• W4296110422 creator A5023165471 @default.
• W4296110422 creator A5023256497 @default.
• W4296110422 creator A5030209500 @default.
• W4296110422 creator A5049333472 @default.
• W4296110422 creator A5052117173 @default.
• W4296110422 creator A5060912538 @default.
• W4296110422 creator A5063727391 @default.
• W4296110422 creator A5064994916 @default.
• W4296110422 creator A5066774199 @default.
• W4296110422 creator A5067435976 @default.
• W4296110422 creator A5069310507 @default.
• W4296110422 creator A5073186349 @default.
• W4296110422 creator A5075134017 @default.
• W4296110422 creator A5082825994 @default.
• W4296110422 date "2022-09-08" @default.
• W4296110422 modified "2023-10-09" @default.
• W4296110422 title "Immune checkpoint inhibitor therapy increases systemic SDF-1, cardiac DAMPs Fibronectin-EDA, S100/Calgranulin, galectine-3, and NLRP3-MyD88-chemokine pathways" @default.
• W4296110422 cites W2016512142 @default.
• W4296110422 cites W2082463141 @default.
• W4296110422 cites W2094366129 @default.
• W4296110422 cites W2100855211 @default.
• W4296110422 cites W2104072610 @default.
• W4296110422 cites W2150048477 @default.
• W4296110422 cites W2163363089 @default.
• W4296110422 cites W2339642721 @default.
• W4296110422 cites W2347141054 @default.
• W4296110422 cites W2516271598 @default.
• W4296110422 cites W2547133566 @default.
• W4296110422 cites W2572174216 @default.
• W4296110422 cites W2589027668 @default.
• W4296110422 cites W2594483928 @default.
• W4296110422 cites W2766430096 @default.
• W4296110422 cites W2788521244 @default.
• W4296110422 cites W2789315292 @default.
• W4296110422 cites W2791800825 @default.
• W4296110422 cites W2792595526 @default.
• W4296110422 cites W2800519327 @default.
• W4296110422 cites W2893646991 @default.
• W4296110422 cites W2914237180 @default.
• W4296110422 cites W2943910007 @default.
• W4296110422 cites W2945464379 @default.
• W4296110422 cites W2946430473 @default.
• W4296110422 cites W2977944907 @default.
• W4296110422 cites W2981790403 @default.
• W4296110422 cites W3003308809 @default.
• W4296110422 cites W3012256530 @default.
• W4296110422 cites W3013344454 @default.
• W4296110422 cites W3036754566 @default.
• W4296110422 cites W3081635153 @default.
• W4296110422 cites W3086240490 @default.
• W4296110422 cites W3091794463 @default.
• W4296110422 cites W3092415006 @default.
• W4296110422 cites W3092560521 @default.
• W4296110422 cites W3093167997 @default.
• W4296110422 cites W3094414272 @default.
• W4296110422 cites W3108805504 @default.
• W4296110422 cites W3109638148 @default.
• W4296110422 cites W3120657480 @default.
• W4296110422 cites W3123572331 @default.
• W4296110422 cites W3139213826 @default.
• W4296110422 cites W3158326626 @default.
• W4296110422 cites W3161113799 @default.
• W4296110422 cites W3165602720 @default.
• W4296110422 cites W3170395917 @default.
• W4296110422 cites W3175392651 @default.
• W4296110422 cites W3188167194 @default.
• W4296110422 cites W3188910902 @default.
• W4296110422 cites W3212115489 @default.
• W4296110422 cites W4200146743 @default.
• W4296110422 cites W4210370153 @default.
• W4296110422 cites W4212814263 @default.
• W4296110422 cites W4213324404 @default.
• W4296110422 cites W4214743418 @default.
• W4296110422 cites W4220949676 @default.
• W4296110422 cites W4225865435 @default.
• W4296110422 cites W4283710615 @default.
• W4296110422 doi "https://doi.org/10.3389/fcvm.2022.930797" @default.
• W4296110422 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/36158826" @default.
• W4296110422 hasPublicationYear "2022" @default.
• W4296110422 type Work @default.
• W4296110422 citedByCount "9" @default.
• W4296110422 countsByYear W42961104222022 @default.
• W4296110422 countsByYear W42961104222023 @default.
• W4296110422 crossrefType "journal-article" @default.
• W4296110422 hasAuthorship W4296110422A5005784207 @default.
• W4296110422 hasAuthorship W4296110422A5023165471 @default.
• W4296110422 hasAuthorship W4296110422A5023256497 @default.
• W4296110422 hasAuthorship W4296110422A5030209500 @default.
• W4296110422 hasAuthorship W4296110422A5049333472 @default.
• W4296110422 hasAuthorship W4296110422A5052117173 @default.
• W4296110422 hasAuthorship W4296110422A5060912538 @default.
• W4296110422 hasAuthorship W4296110422A5063727391 @default.
• W4296110422 hasAuthorship W4296110422A5064994916 @default.
• W4296110422 hasAuthorship W4296110422A5066774199 @default.
• W4296110422 hasAuthorship W4296110422A5067435976 @default.
• W4296110422 hasAuthorship W4296110422A5069310507 @default.
• W4296110422 hasAuthorship W4296110422A5073186349 @default.

• next