Evidence map›Paper›PMID 20628203›Full record

ArticleThe Journal of clinical investigation2010

Angiotensin II sustains brain inflammation in mice via TGF-beta.

Tobias V Lanz, Zhaoqing Ding, Peggy P Ho, Jian Luo, Ankur N Agrawal, Hrishikesh Srinagesh, Robert Axtell, Hui Zhang, Michael Platten, Tony Wyss-Coray and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 1 pooled it
6.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

124 citing papers in PubMed, 1 synthesis or guideline pooled it, 198 citations in OpenAlex.

  1. Systematically exploring repurposing effects of antihypertensives.Pharmacoepidemiology and drug safety · 2022
    Pooled it
  2. Trial
  3. Review
  4. Microglial activation and RAS signaling: a dual-edged sword in neuroinflammation.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Review
  5. Article
  6. Article
  7. Regulatory network analysis ofbioRxiv : the preprint server for biology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. The Angiotensin ATPharmacological reviews · 2022
    Review
  18. Innate immune suppression by SARS-CoV-2 mRNA vaccinations: The role of G-quadruplexes, exosomes, and MicroRNAs.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2022
    Article
  19. Review
  20. Review

64 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Tobias V LanzDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California, USA.
Zhaoqing Ding
Peggy P Ho
Jian Luo
Ankur N Agrawal
Hrishikesh Srinagesh
Robert Axtell
Hui Zhang
Michael Platten
Tony Wyss-Coray
Lawrence Steinman
Stanford University · USTranslational Research in Oncology · FR

Funding

MOLECULAR &CELLULAR IMMUNOBIOLOGYT32AI007290 · NIAID · STANFORD UNIVERSITY · PI Sean Curtis Bendall, Olivia M Martinez · 1985 to 2026
$27.0M
Multiple Sclerosis Society 835NIAID NIH HHS T32 AI007290
6 · The paper itself

Abstract

The renin-angiotensin-aldosterone system (RAAS) is a key hormonal system regulating blood pressure. However, expression of RAAS components has recently been detected in immune cells, and the RAAS has been implicated in several mouse models of autoimmune disease. Here, we have identified Ang II as a paracrine mediator, sustaining inflammation in the CNS in the EAE mouse model of MS via TGF-beta. Ang II type 1 receptors (AT1Rs) were found to be primarily expressed in CNS-resident cells during EAE. In vitro, astrocytes and microglia responded to Ang II treatment by inducing TGF-beta expression via a pathway involving the TGF-beta-activating protease thrombospondin-1 (TSP-1). TGF-beta upregulation in astrocytes and microglia during EAE was blocked with candesartan (CA), an inhibitor of AT1R. Treatment of EAE with CA ameliorated paralysis and blunted lymphocyte infiltration into the CNS, outcomes that were also seen with genetic ablation of AT1Ra and treatment with an inhibitor of TSP-1. These data suggest that AT1R antagonists, frequently prescribed as antihypertensives, may be useful to interrupt this proinflammatory, CNS-specific pathway in individuals with MS.

Indexed as

Angiotensin IIAnimalsBenzimidazolesBiphenyl CompoundsCells, CulturedChronic DiseaseEncephalomyelitis, Autoimmune, ExperimentalFemaleMiceMice, Inbred C57BLReceptor, Angiotensin, Type 1Renin-Angiotensin SystemSignal TransductionTetrazolesThrombospondin 1Transforming Growth Factor betaAngiotensin IIBenzimidazolesBiphenyl CompoundscandesartanReceptor, Angiotensin, Type 1TetrazolesThrombospondin 1Transforming Growth Factor beta

Identifiers

PMID20628203
PMCPMC2912186
OpenAlexW2064623974

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.