Evidence map›Paper›PMID 40205453›Full record

ArticleCardiovascular research2025

Beta 2 adrenergic receptor gene methylation activates innate lymphoid cells to drive hypertension in lymphocyte deficient hosts.

Wei Chen, Sara Perrotta, Liang Xiao, Lorenzo Carnevale, Marwa A Abd-ElDayem, Elizabeth M Hennen, Luis Miguel Rivera-Medina, David M Patrick, Mingfang Ao, Fabio Pallante and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

20 authors.

Wei ChenDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Sara PerrottaDepartment of Angiocardioneurology and Translational Medicine, Unit of Neuro and Cardiovascular Pathophysiology, IRCCS Neuromed, Via dell'Elettronica, Pozzilli 86077, Italy.ORCID 0000-0002-2903-3223
Liang XiaoDisease Center, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, PR China.
Lorenzo CarnevaleDepartment of Angiocardioneurology and Translational Medicine, Unit of Neuro and Cardiovascular Pathophysiology, IRCCS Neuromed, Via dell'Elettronica, Pozzilli 86077, Italy.ORCID 0000-0002-6422-8253
Marwa A Abd-ElDayemDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Elizabeth M HennenDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Luis Miguel Rivera-MedinaDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
David M PatrickDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Mingfang AoDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.
Fabio PallanteDepartment of Angiocardioneurology and Translational Medicine, Unit of Neuro and Cardiovascular Pathophysiology, IRCCS Neuromed, Via dell'Elettronica, Pozzilli 86077, Italy.
Azzurra ZonfrilliDepartment of Molecular Medicine, Sapienza University of Rome, Viale Regina Elena, 291, Rome 00161, Italy.
Shilin ZhaoDepartment of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, USA.
Agnese MigliaccioDepartment of Angiocardioneurology and Translational Medicine, Unit of Neuro and Cardiovascular Pathophysiology, IRCCS Neuromed, Via dell'Elettronica, Pozzilli 86077, Italy.
Lan LanDisease Center, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang Province, PR China.
Stefania FardellaDepartment of Angiocardioneurology and Translational Medicine, Unit of Neuro and Cardiovascular Pathophysiology, IRCCS Neuromed, Via dell'Elettronica, Pozzilli 86077, Italy.
Giuseppe SciumèDepartment of Molecular Medicine, Sapienza University of Rome, Viale Regina Elena, 291, Rome 00161, Italy.
Francesco MastroiacovoDepartment of Angiocardioneurology and Translational Medicine, Unit of Neuro and Cardiovascular Pathophysiology, IRCCS Neuromed, Via dell'Elettronica, Pozzilli 86077, Italy.ORCID 0000-0001-5704-8599
Giuseppe LemboDepartment of Angiocardioneurology and Translational Medicine, Unit of Neuro and Cardiovascular Pathophysiology, IRCCS Neuromed, Via dell'Elettronica, Pozzilli 86077, Italy.ORCID 0000-0002-3510-223X
Daniela CarnevaleDepartment of Angiocardioneurology and Translational Medicine, Unit of Neuro and Cardiovascular Pathophysiology, IRCCS Neuromed, Via dell'Elettronica, Pozzilli 86077, Italy.ORCID 0000-0002-5016-3161
David G HarrisonDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, TN, USA.

Funding

American Heart Association Scientist Development 17SDG33670829American Heart Association Scientist Development T32HL144446Italian Ministry of Health 'Ricerca Corrente'National Institute of Health 1R01HL134895-02National Institute of Health 5P01HL129941-03National Institute of Health 5R35HL140016-02Veterans Affairs Biomedical Laboratory Research Career Development IK2BX005376
6 · The paper itself

Abstract

aimsT cells contribute to hypertension; however, hypertension occurs in settings of T cell deficiency. METHODS AND

resultsWe studied two colonies of T/B cell-deficient RAG-1-/- mice with disparate responses to angiotensin II, being one protected from blood pressure increase and the other one responsive. This difference depends on the capability of hypertensive RAG-1-/- mice to expand natural killer and innate lymphoid cells (NK/ILCs) that produce pro-hypertensive cytokines. This process is regulated by the DNA methylation status of the β2 adrenergic receptor (β2-AdR). Angiotensin II caused blood pressure elevation in T and NK/ILCs-deficient mice only when either T or NK/ILCs cells were adoptively reconstituted. Additional studies showed NK cell expansion in humans that underwent B cell depletion, and this was augmented in those with hypertension.

conclusionsThese findings illustrate that the modulation of NK/ILCs activation by adrenergic signalling governs an escape mechanism in lymphocyte-deficient host, enabling the development of hypertension.

Indexed as

Blood PressureB-LymphocytesDNA MethylationHypertensionImmunity, InnateKiller Cells, NaturalReceptors, Adrenergic, beta-2T-LymphocytesAngiotensin IIAnimalsCells, CulturedCytokinesDisease Models, AnimalHomeodomain ProteinsHumansMaleADRB2 protein, humanADRB2 protein, mouseAngiotensin IICytokinesHomeodomain ProteinsRAG-1 proteinReceptors, Adrenergic, beta-2Adoptive transferAngiotensin IIBeta 2 adrenergic receptorHypertensionIL-17AInnate lymphoid cellsMethylationNatural killer cells

Identifiers

PMID40205453
PMCPMC12101357

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.