Evidence map›Paper›PMID 27187688›Full record

ArticlePloS one2016

Telmisartan Modulates Glial Activation: In Vitro and In Vivo Studies.

Nofar Torika, Keren Asraf, Abraham Danon, Ron N Apte, Sigal Fleisher-Berkovich

2 registry-linked trialsOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
5.2field-weighted citation impact, top 4% 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.

NCT06168487 phase1recruitingnot on this mapstarted 2024, after this paper: background citation

Phase I Non-Randomized, Unblinded, Single-Center Trial of Oral Telmisartan Alone or Combined With Selected Standard of Care Therapies for Prostate Cancer

TypeinterventionalSponsorTyler J CurielRan2024 to 2027Enrolled36ConditionsProstate CancerArmsTelmisartan, Standard of Care Regimen
NCT06815497 phase2recruitingnot on this mapstarted 2026, after this paper: background citation

Phase II Non-Randomized, Unblinded, Single-Center Trial of Telmisartan in Combination With Cytotoxic Regimens in Platinum-Resistant Ovarian Cancer Versus Historical Best Supportive Care

TypeinterventionalSponsorTyler J CurielRan2026 to 2029Enrolled33ConditionsOvarian CancerArmsTelmisartan
3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 62 citations in OpenAlex.

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  15. Recent Advances in the Endogenous Brain Renin-Angiotensin System and Drugs Acting on It.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2021
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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

5 authors at 1 institution in 1 country.

Nofar TorikaDepartment of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva P.O.B 653, Israel.
Keren AsrafDepartment of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva P.O.B 653, Israel.
Abraham DanonDepartment of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva P.O.B 653, Israel.
Ron N ApteDepartment of Microbiology and Immunology, Ben-Gurion University of the Negev, Beer-Sheva P.O.B 653, Israel.
Sigal Fleisher-BerkovichDepartment of Clinical Biochemistry and Pharmacology, Ben-Gurion University of the Negev, Beer-Sheva P.O.B 653, Israel.
Ben-Gurion University of the Negev · IL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The circulating renin-angiotensin system (RAS), including the biologically active angiotensin II, is a fundamental regulatory mechanism of blood pressure conserved through evolution. Angiotensin II components of the RAS have also been identified in the brain. In addition to pro-inflammatory cytokines, neuromodulators, such as angiotensin II can induce (through angiotensin type 1 receptor (AT1R)) some of the inflammatory actions of brain glial cells and influence brain inflammation. Moreover, in Alzheimer's disease (AD) models, where neuroinflammation occurs, increased levels of cortical AT1Rs have been shown. Still, the precise role of RAS in neuroinflammation is not completely clear. The overall aim of the present study was to elucidate the role of RAS in the modulation of glial functions and AD pathology. To reach this goal, the specific aims of the present study were a. to investigate the long term effect of telmisartan (AT1R blocker) on tumor necrosis factor-α (TNF-α), interleukin 1-β (IL1-β) and nitric oxide (NO) release from glial cells. b. to examine the effect of intranasally administered telmisartan on amyloid burden and microglial activation in 5X familial AD (5XFAD) mice. Telmisartan effects in vivo were compared to those of perindopril (angiotensin converting enzyme inhibitor). Long-term-exposure of BV2 microglia to telmisartan significantly decreased lipopolysaccharide (LPS) -induced NO, inducible NO synthase, TNF-α and IL1-β synthesis. The effect of Telmisartan on NO production in BV2 cells was confirmed also in primary neonatal rat glial cells. Intranasal administration of telmisartan (1 mg/kg/day) for up to two months significantly reduced amyloid burden and CD11b expression (a marker for microglia) both in the cortex and hipoccampus of 5XFAD. Based on the current view of RAS and our data, showing reduced amyloid burden and glial activation in the brains of 5XFAD transgenic mice, one may envision potential intervention with the progression of glial activation and AD by using AT1R blockers.

Indexed as

Administration, IntranasalAlzheimer DiseaseAngiotensin II Type 1 Receptor BlockersAnimalsBenzimidazolesBenzoatesCell LineCells, CulturedFemaleMaleMiceMice, TransgenicMicrogliaNeurogliaNitric OxideRatsAngiotensin II Type 1 Receptor BlockersBenzimidazolesBenzoatesNitric OxideTelmisartan

Identifiers

PMID27187688
PMCPMC4871324
OpenAlexW2402393879

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.