Evidence map›Paper›PMID 29922176›Full record

ArticleFrontiers in physiology2018

Transient Receptor Potential Vanilloid 1 Expression Mediates Capsaicin-Induced Cell Death.

Ricardo Ramírez-Barrantes, Claudio Córdova, Sebastian Gatica, Belén Rodriguez, Carlo Lozano, Ivanny Marchant, Cesar Echeverria, Felipe Simon, Pablo Olivero

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
2.9field-weighted citation impact, top 10% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 42 citations in OpenAlex.

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  19. Gallic Acid Inhibits Mesaconitine-Activated TRPV1-Channel-Induced Cardiotoxicity.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  20. Optogenetic control of cancer cell survival in ChR2-transfected HeLa cells.International journal of experimental pathology · 2021
    Article
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

9 authors at 3 institutions in 1 country.

Ricardo Ramírez-BarrantesLaboratorio de Estructura y Función Celular, Escuela de Medicina, Facultad de Medicina, Universidad de Valparaíso, Valparaíso, Chile.
Claudio CórdovaLaboratorio de Estructura y Función Celular, Escuela de Medicina, Facultad de Medicina, Universidad de Valparaíso, Valparaíso, Chile.
Sebastian GaticaDepartamento de Ciencias Biologicas, Facultad de Ciencias de la Vida, Universidad Andres Bello, Santiago, Chile.
Belén RodriguezLaboratorio de Estructura y Función Celular, Escuela de Medicina, Facultad de Medicina, Universidad de Valparaíso, Valparaíso, Chile.
Carlo LozanoLaboratorio de Estructura y Función Celular, Escuela de Medicina, Facultad de Medicina, Universidad de Valparaíso, Valparaíso, Chile.
Ivanny MarchantLaboratorio de Estructura y Función Celular, Escuela de Medicina, Facultad de Medicina, Universidad de Valparaíso, Valparaíso, Chile.
Cesar EcheverriaCentro Integrativo de Biología y Química Aplicada, Universidad Bernardo O'Higgins, Santiago, Chile.
Felipe SimonDepartamento de Ciencias Biologicas, Facultad de Ciencias de la Vida, Universidad Andres Bello, Santiago, Chile.
Pablo OliveroLaboratorio de Estructura y Función Celular, Escuela de Medicina, Facultad de Medicina, Universidad de Valparaíso, Valparaíso, Chile.
University of Valparaíso · CLUniversidad Andrés Bello · CLUniversidad Bernardo O'Higgins · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The transient receptor potential (TRP) ion channel family consists of a broad variety of non-selective cation channels that integrate environmental physicochemical signals for dynamic homeostatic control. Involved in a variety of cellular physiological processes, TRP channels are fundamental to the control of the cell life cycle. TRP channels from the vanilloid (TRPV) family have been directly implicated in cell death. TRPV1 is activated by pain-inducing stimuli, including inflammatory endovanilloids and pungent exovanilloids, such as capsaicin (CAP). TRPV1 activation by high doses of CAP (>10 μM) leads to necrosis, but also exhibits apoptotic characteristics. However, CAP dose-response studies are lacking in order to determine whether CAP-induced cell death occurs preferentially via necrosis or apoptosis. In addition, it is not known whether cytosolic Ca

Indexed as

calciumcapsaicincell deathmitochondrianecrosisTRPV1

Identifiers

PMID29922176
PMCPMC5996173
OpenAlexW2807210425

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.