Evidence map›Paper›PMID 28724611›Full record

ReviewAmerican journal of physiology. Renal physiology2017

Tumor necrosis factor-α, kidney function, and hypertension.

Eamonn Mehaffey, Dewan S A Majid

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed, 2 pooled it
8.0field-weighted citation impact, top 1% 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

94 citing papers in PubMed, 2 syntheses or guidelines pooled it, 173 citations in OpenAlex.

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  15. Recent advances on immunity and hypertension: the new cells on the kidney block.American journal of physiology. Renal physiology · 2025
    Review
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34 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

2 authors at 1 institution in 1 country.

Eamonn MehaffeyDepartment of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana.
Dewan S A MajidDepartment of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University School of Medicine, New Orleans, Louisiana majid@tulane.edu.
Tulane University · US

Funding

Translational Research in Hypertension and Renal BiologyP30GM103337 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2012 to 2016
$5.8M
Superoxide and nitric Oxide Interactions in the KidneyR01HL066432 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI MAJID, DEWAN SYED ABDUL · 2001 to 2012
$3.0M
NHLBI NIH HHS R01 HL066432NIGMS NIH HHS P30 GM103337
6 · The paper itself

Abstract

Hypertension is considered to be a low-grade inflammatory condition characterized by the presence of various proinflammatory cytokines. Tumor necrosis factor-α (TNF-α) is a constituent of the proinflammatory cytokines that is associated with salt-sensitive hypertension (SSH) and related renal injury. Elevated angiotensin II (ANG II) and other factors such as oxidative stress conditions promote TNF-α formation. Many recent studies have provided evidence that TNF-α exerts a direct renal action by regulating hemodynamic and excretory function in the kidney. The cytokine incites a strong natriuretic response and plays a part in regulation of the intrarenal renin-angiotensin system. The exact mechanistic role of TNF-α in the development of SSH is as yet poorly understood. While TNF-α antagonism has been shown to attenuate hypertensive responses in many hypertensive animal models, contrasting findings demonstrate that the direct systemic administration of TNF-α usually induces hypotensive as well as natriuretic responses, indicating a counterregulatory role of TNF-α in SSH. Differential activities of two cell surface receptors of TNF-α (receptor type 1 and type 2) may explain the contradictory functions of TNF-α in the setting of hypertension. This short review will evaluate ongoing research studies that investigate the action of TNF-α within the kidney and its role as an influential pathophysiological variable in the development of SSH and renal injury. This information may help to develop specific TNF-α receptor targeting as an effective treatment strategy in this clinical condition.

Indexed as

Blood PressureAnimalsHumansHypertensionInflammationInflammation MediatorsKidneyReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IIRenin-Angiotensin SystemSignal TransductionSodium Chloride, DietaryTumor Necrosis Factor-alphaInflammation MediatorsReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type IISodium Chloride, DietaryTumor Necrosis Factor-alphainflammatory cytokinesnatriuresisrenin-angiotensin systemTNF-α

Identifiers

PMID28724611
PMCPMC5668589
OpenAlexW2738381851

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.