Evidence map›Paper›PMID 23637043›Full record

ArticleClinical and vaccine immunology : CVI2013

TRPV1 ablation aggravates inflammatory responses and organ damage during endotoxic shock.

Youping Wang, Donna H Wang

Open access · diamondAbstract read
In one paragraph

Article in Clinical and vaccine immunology : CVI, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.5field-weighted citation impact, top 20% 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

20 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. TRPV1: The key bridge in neuroimmune interactions.Journal of intensive medicine · 2024
    Review
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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

2 authors at 2 institutions in 2 countries.

Youping WangCentral Laboratory and Division of Cardiology, First Affiliated Hospital, Henan University of Traditional Chinese Medicine, Zhengzhou, China.
Donna H Wang
First Affiliated Hospital of Henan University of Traditional Chinese Medicine · CNMichigan State University · US

Funding

Vanilloid Sensitive Sensory Nerves and Salt SensitivityR01HL073287 · NHLBI · MICHIGAN STATE UNIVERSITY · PI WANG, DONNA H · 2004 to 2011
$2.7M
Molecular Sensing of Sodium Homeostasis: Anandamide RoleR01DK067620 · NIDDK · MICHIGAN STATE UNIVERSITY · PI WANG, DONNA H · 2005 to 2009
$1.4M
RENAL ANGIOTENSIN II RECEPTOR AND SODIUM INTAKER01HL057853 · NHLBI · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI WANG, DONNA H · 1998 to 2007
$1.1M
NHLBI NIH HHS HL-57853NHLBI NIH HHS HL-73287NHLBI NIH HHS R01 HL057853NHLBI NIH HHS R01 HL073287NIDDK NIH HHS DK67620NIDDK NIH HHS R01 DK067620
6 · The paper itself

Abstract

To test the hypothesis that ablation of transient receptor potential vanilloid type 1 (TRPV1) channels leads to exacerbated inflammatory responses and organ damage during endotoxic shock, lipopolysaccharide (LPS; 5 million endotoxin units/kg of body weight) was injected intraperitoneally (i.p.) into wild-type (WT) and TRPV1-null mutant (TRPV1(-/-)) mice. Mean arterial pressure and heart rate, determined by radiotelemetry, were severely depressed after LPS injection into WT and TRPV1(-/-) mice, with no distinction between the two strains. At 24 h after LPS injection, renal glomerular hypercellularity and hepatocellular injury were observed in both strains, accompanying further elevated serum levels of creatinine and alanine aminotransferase in TRPV1(-/-) mice compared to those in WT mice. At 6 or 24 h after LPS injection, neutrophil recruitment into kidneys and livers, serum cytokine (tumor necrosis factor alpha [TNF-α], interleukin 1β [IL-1β], IL-6) and renal chemokine (KC, macrophage inflammatory protein 2 [MIP-2]) levels, and renal VCAM-1 and ICAM-1 expression were greater in TRPV1(-/-) mice than WT mice. In addition, increased plasma calcitonin gene-related peptide (CGRP) levels observed in WT mice 6 h after LPS injection were absent in TRPV1(-/-) mice. Thus, TRPV1 ablation aggravates inflammatory responses, including neutrophil infiltration, proinflammatory cytokine production, and adhesion molecule expression, leading to intensified organ damage during endotoxic shock in the absence of worsened circulatory failure. The data indicate that TRPV1 activation may attenuate endotoxin-induced organ damage, possibly via its anti-inflammatory action rather than alteration of hemodynamics.

Indexed as

AnimalsHepatitisHistocytochemistryInjections, IntraperitonealLipopolysaccharidesMiceMice, KnockoutNephritisShock, SepticTRPV Cation ChannelsLipopolysaccharidesTRPV1 protein, mouseTRPV Cation Channels

Identifiers

PMID23637043
PMCPMC3697449
OpenAlexW2127342358

What OpenQuestion holds

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Registered trials

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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.