Evidence map›Paper›PMID 32498083›Full record

ReviewAmerican journal of hypertension2020

TNFα and Reactive Oxygen Signaling in Vascular Smooth Muscle Cells in Hypertension and Atherosclerosis.

Fred S Lamb, Hyehun Choi, Michael R Miller, Ryan J Stark

Open access · greenAbstract readReview
In one paragraph

Review in American journal of hypertension, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  19. Hypertension facilitates age-related diseases. ~ Is hypertension associated with a wide variety of diseases?~.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  20. 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

4 authors at 1 institution in 1 country.

Fred S LambDivision of Pediatric Critical Care, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Hyehun ChoiDivision of Pediatric Critical Care, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Michael R MillerDivision of Pediatric Critical Care, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Ryan J StarkDivision of Pediatric Critical Care, Department of Pediatrics, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Vanderbilt University Medical Center · US

Funding

Ductus Arteriosus Regulation by Anion ChannelsR01HL128386 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI LAMB, FRED S, REESE, JOHN JEFFREY · 2016 to 2019
$2.3M
Vanderbilt Hypertension and Blood Pressure Regulation ProgramT32HL144446 · NHLBI · VANDERBILT UNIVERSITY · PI HARRISON, DAVID G · 2019 to 2023
$1.7M
Prevention of Endothelial Injury by Toll-like Receptor 4 ModulatorsK08GM117367 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI STARK, RYAN J · 2015 to 2018
$734k
NHLBI NIH HHS R01 HL128386NHLBI NIH HHS T32 HL144446NIGMS NIH HHS K08 GM117367
6 · The paper itself

Abstract

Hypertension and atherosclerosis, the predecessors of stroke and myocardial infarction, are chronic vascular inflammatory reactions. Tumor necrosis factor alpha (TNFα), the "master" proinflammatory cytokine, contributes to both the initiation and maintenance of vascular inflammation. TNFα induces reactive oxygen species (ROS) production which drives the redox reactions that constitute "ROS signaling." However, these ROS may also cause oxidative stress which contributes to vascular dysfunction. Mice lacking TNFα or its receptors are protected against both acute and chronic cardiovascular injury. Humans suffering from TNFα-driven inflammatory conditions such as rheumatoid arthritis and psoriasis are at increased cardiovascular risk. When treated with highly specific biologic agents that target TNFα signaling (Etanercept, etc.) they display marked reductions in that risk. The ability of TNFα to induce endothelial dysfunction, often the first step in a progression toward serious vasculopathy, is well recognized and has been reviewed elsewhere. However, TNFα also has profound effects on vascular smooth muscle cells (VSMCs) including a fundamental change from a contractile to a secretory phenotype. This "phenotypic switching" promotes proliferation and production of extracellular matrix proteins which are associated with medial hypertrophy. Additionally, it promotes lipid storage and enhanced motility, changes that support the contribution of VSMCs to neointima and atherosclerotic plaque formation. This review focuses on the role of TNFα in driving the inflammatory changes in VSMC biology that contribute to cardiovascular disease. Special attention is given to the mechanisms by which TNFα promotes ROS production at specific subcellular locations, and the contribution of these ROS to TNFα signaling.

Indexed as

AnimalsAtherosclerosisHumansHypertensionMuscle, Smooth, VascularMyocytes, Smooth MuscleReactive Oxygen SpeciesSignal TransductionTumor Necrosis Factor-alphaReactive Oxygen SpeciesTumor Necrosis Factor-alphaatherosclerosisblood pressurehypertensionLRRC8ANox1reactive oxygen signalingTNFαvascular smooth muscle

Identifiers

PMID32498083
PMCPMC7577645
OpenAlexW3033452052

What Socratic 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 Socratic graph.