Evidence map›Paper›PMID 42080133›Full record

ArticleiScience2026

Peptidylarginine deiminase 4 is a differential regulator of salt-sensitive and salt-resistant hypertension.

Xue Mei, Piu Saha, Blair Mell, Sareh Zeydabadinejad, Beng San Yeoh, Amira Gohara, Matam Vijay-Kumar, Bina Joe

Abstract read
In one paragraph

Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Xue MeiMicrobiome Consortium, Center for Hypertension & Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
Piu SahaMicrobiome Consortium, Center for Hypertension & Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
Blair MellMicrobiome Consortium, Center for Hypertension & Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
Sareh ZeydabadinejadMicrobiome Consortium, Center for Hypertension & Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
Beng San YeohMicrobiome Consortium, Center for Hypertension & Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
Amira GoharaDepartment of Pathology, University of Toledo Medical Center, Toledo, OH, USA.
Matam Vijay-KumarMicrobiome Consortium, Center for Hypertension & Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.
Bina JoeMicrobiome Consortium, Center for Hypertension & Precision Medicine, Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, OH, USA.

Funding

Role of neutrophil extracellular traps (NETs) in Inflammatory bowel diseaseR01DK134053 · NIDDK · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI MATAM VIJAY-KUMAR · 2023 to 2026
$1.7M
NIDDK NIH HHS R01 DK134053
6 · The paper itself

Abstract

Neutrophils contribute to immune surveillance by releasing neutrophil extracellular traps (NETs) through NETosis. While essential, dysregulated NETosis is linked to pathology. We examined its role in salt-sensitive versus salt-resistant hypertension using Dahl rat models. Hypertensive Dahl S rats, but not normotensive Dahl R rats, showed increased NETosis, higher neutrophil counts, and chronic low-grade inflammation. Inhibiting NETosis with DNase I or by the genetic deletion of peptidyl arginine deiminase (Pad4) exacerbated blood pressure (BP) in S rats, suggesting NETosis protects against salt-sensitive hypertension. Pad4 deletion also caused neutropenia, reduced reactive oxygen species, and exaggerated BP elevation under a high-salt diet. In contrast, Pad4 deletion in R rats lowered systolic BP regardless of diet, indicating NETosis supports BP homeostasis in normotension. These findings highlight the context-dependent role of NETosis in BP regulation, with NETs acting as a protective mechanism in salt-sensitive hypertension.

Indexed as

diseaseimmunologyphysiology

Identifiers

PMID42080133
PMCPMC13129381

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.