| Literature DB >> 34233704 |
Junjun Yin1, Jiayang Wan2, Jiaqi Zhu1, Guoying Zhou1, Yuming Pan1, Huifen Zhou3.
Abstract
BACKGROUND: Sterile inflammation is a key pathological process in stroke. Inflammasome activation has been implicated in various inflammatory diseases, including ischemic stroke and hemorrhagic stroke. Hence, targeting inflammasomes is a promising approach for the treatment of stroke.Entities:
Keywords: Bibliometric; Global trends; Hemorrhagic stroke; Inflammasomes; Ischemic stroke; Mitochondrial dysfunction
Year: 2021 PMID: 34233704 PMCID: PMC8265129 DOI: 10.1186/s13020-021-00464-9
Source DB: PubMed Journal: Chin Med ISSN: 1749-8546 Impact factor: 5.455
Fig. 1Details of filtrating the data. A manual review was performed on the original search on WOSCC to filter out documents that are not related to inflammasomes in stroke
Fig. 2A The hollow pie chart illustrates the proportion of document number of each type. B The line chart shows the number of papers on inflammasome and stroke research published and the exponential trend line over time (the black line and red dotted line)
The TOP 10 highly cited articles
| Rank | Title | Total Citations | Authors | Source | Year | Type |
|---|---|---|---|---|---|---|
| 1 | Pyroptosis: host cell death and inflammation | 1171 | Bergsbaken T, Fink SL et al | NATURE REVIEWS MICROBIOLOGY Volume 7, issue 2, pages 99–109 | 2009 | Review |
| 2 | Interleukin-1 beta inhibition and the prevention of recurrent cardiovascular events: Rationale and Design of the Canakinumab Anti-inflammatory Thrombosis Outcomes Study (CANTOS) | 574 | Ridker PM, Thuren T et al | AMERICAN HEART JOURNAL Volume162, issue 4, pages 597–605 | 2011 | Article |
| 3 | Inflammasomes in the CNS | 306 | Walsh JG, Muruve DA et al | NATURE REVIEWS NEUROSCIENCE Volume 15, issue 2, pages 84–97 | 2014 | Review |
| 4 | Intravenous immunoglobulin suppresses NLRP1 and NLRP3 inflammasome-mediated neuronal death in ischemic stroke | 206 | Fann DYW, Lee SY et al | CELL DEATH AND DISEASE Volume 4, e790 | 2013 | Article |
| 5 | P2X7 receptor: an emerging target in central nervous system diseases | 197 | Sperlagh B, Illes P et al | TRENDS IN PHARMACOLOGICAL SCIENCES Volume 35, issue 10, pages 537–547 | 2014 | Review |
| 6 | Inhibition of the inflammasome complex reduces the inflammatory response after thromboembolic stroke in mice | 195 | Abulafia DP,Vaccari, JPD et al | JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM Volume 29, issue 3, pages 534–544 | 2009 | Article |
| 7 | NLRP3 deficiency ameliorates neurovascular damage in experimental ischemic stroke | 182 | Yang F, Wang ZY et al | JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM Volume 34, issue 4, pages 660–667 | 2014 | Article |
| 8 | Release and activity of histone in diseases | 173 | Chen R, Kang R et al | CELL DEATH AND DISEASE Volume 5, e1370 | 2014 | Review |
| 9 | Functions and mechanisms of microglia/macrophages in neuroinflammation and neurogenesis after stroke | 165 | Xiong XY, Liu L et al | PROGRESS IN NEUROBIOLOGY Volume 142, pages 23–44 | 2016 | Review |
| 10 | Activation and regulation of cellular inflammasomes: gaps in our knowledge for central nervous system injury | 153 | Vaccari JPD, Dietrich WD et al | JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM. Volume 34, issue 3, pages 369–375 | 2014 | Review |
The TOP 10 Journals of publications and co-cited journals
| Rank | Journals | Publications | Impact factor | Co-cited journals | Citations | Impact factor |
|---|---|---|---|---|---|---|
| 1 | J NEUROINFLAMM | 28 | 5.793 | STROKE | 846 | 7.190 |
| 2 | INT IMMUNOPHARMACOL | 12 | 3.943 | J CEREBR BLOOD F MET | 798 | 5.681 |
| 3 | INT J MOL SCI | 12 | 4.556 | NATURE | 680 | 42.778 |
| 4 | BIOCHEM BIOPH RES CO | 10 | 2.985 | P NATL ACAD SCI USA | 599 | 9.412 |
| 5 | EXP NEUROL | 10 | 4.691 | J NEUROSCI | 556 | 5.673 |
| 6 | CNS NEUROSCI THER | 9 | 4.074 | J NEUROINFLAMM | 532 | 5.793 |
| 7 | MOL NEUROBIOL | 9 | 4.500 | J BIOL CHEM | 515 | 4.238 |
| 8 | J CEREBR BLOOD F MET | 8 | 5.681 | PLOS ONE | 475 | 2.740 |
| 9 | STROKE | 8 | 7.190 | J IMMUNOL | 470 | 4.886 |
| 10 | FRONT CELL NEUROSCI | 7 | 3.921 | CELL | 392 | 38.637 |
The TOP 10 authors and co-cited author
| Rank | Authors | Citations# | H-index* | Co-cited authors | Citations |
|---|---|---|---|---|---|
| 1 | KEANE RW | 479 | 38 | FANN DYW | 214 |
| 2 | VACCARI JPD | 441 | 25 | MARTINON F | 126 |
| 3 | DIETRICH WD | 412 | 91 | YANG F | 99 |
| 4 | BROUGH D | 367 | 48 | LAMKANFI M | 92 |
| 5 | CHEN S | 361 | 15 | ZHOU RB | 81 |
| 6 | ZHANG JH | 308 | 73 | VACCARI JPD | 74 |
| 7 | ARUMUGAM TV | 304 | 56 | ABULAFIA DP | 71 |
| 8 | ALLAN SM | 289 | 45 | SCHRODER K | 70 |
| 9 | ISHRAT T | 184 | 32 | DENES A | 68 |
| 10 | ZHAO J | 180 | 13 | HENEKA MT | 67 |
#Citations refer to the sum of citations that each author’s articles related to “inflammasomes in stroke” research have totally received
*H-Index, a scientific evaluation of influence, is extracted from WOSCC
Fig. 3Co-authorship country analysis. The top 5 citations countries and the country co-authorship overlay visualization map. The color of each circle indicates the average publication year for the country, according to the color gradient shown in the lower right corner
Fig. 4Co-authorship institutions analysis. The top 5 citations institutions and the institution co-authorship overlay visualization map. The color of each circle indicates the average publication year for the country, according to the color gradient shown in the lower right corner
Fig. 5Author keyword co-occurrence analysis. Author keywords are labeled. The color of each circle indicates the average year when the keyword appeared in articles, according to the color gradient color in the lower right corner. The distance between any two circles is indicative of their co-occurrence link, and the thickness of the connecting line indicates the strength of the link
Fig. 6Summary of main literature. A Ischemic stroke (including CVT, GCI, FCI and NHIBD) and hemorrhagic stroke (including SAH and ICH) are major types of stroke. The full name is marked in the "abbreviations" section. B DAMPs and PAMPs lead to dysregulation of extracellular pH, efflux of Ca2+, failure of K+/Na+ ATPases, mitochondrial dysfunction, and DNA damage, which further more result in inflammasomes are activated. C Inflammasomes in general are expressed in microglia, astrocytes, neurons, and endothelial cells. Activation of inflammasomes releases excessive inflammatory cytokines, including IL-1β, IL-18, IL-6 and TNF-α, and finally contributes to cell death