Evidence map›Paper›PMID 38972305›Full record

ArticleKidney & blood pressure research2024

Inflammatory Alterations to Renal Lymphatic Endothelial Cell Gene Expression in Mouse Models of Hypertension.

Justin G McDermott, Bethany L Goodlett, Heidi A Creed, Shobana Navaneethabalakrishnan, Joseph M Rutkowski, Brett M Mitchell

Abstract read
In one paragraph

Article in Kidney & blood pressure research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. The endothelium response to kidney injury.Nature reviews. Nephrology · 2026
    Review
  2. Article
  3. 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

6 authors.

Justin G McDermottDepartment of Medical Physiology, Texas A&M University School of Medicine, Bryan, Texas, USA.
Bethany L GoodlettDepartment of Medical Physiology, Texas A&M University School of Medicine, Bryan, Texas, USA.
Heidi A CreedDepartment of Medical Physiology, Texas A&M University School of Medicine, Bryan, Texas, USA.
Shobana NavaneethabalakrishnanDepartment of Medical Physiology, Texas A&M University School of Medicine, Bryan, Texas, USA.
Joseph M RutkowskiDepartment of Medical Physiology, Texas A&M University School of Medicine, Bryan, Texas, USA.
Brett M MitchellDepartment of Medical Physiology, Texas A&M University School of Medicine, Bryan, Texas, USA.

Funding

Lymphatics and lymphangiogenesis in kidney function and inflammationR01DK119497 · NIDDK · TEXAS A&M UNIVERSITY · PI RUTKOWSKI, JOSEPH MICHAEL · 2020 to 2024
$2.1M
Role of Renal Lymphatics in Blood Pressure RegulationR01DK120493 · NIDDK · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI MITCHELL, BRETT M · 2019 to 2022
$1.6M
NIDDK NIH HHS R01 DK119497NIDDK NIH HHS R01 DK120493
6 · The paper itself

Abstract

introductionHypertension (HTN) is a major cardiovascular disease that can cause and be worsened by renal damage and inflammation. We previously reported that renal lymphatic endothelial cells (LECs) increase in response to HTN and that augmenting lymphangiogenesis in the kidneys reduces blood pressure and renal pro-inflammatory immune cells in mice with various forms of HTN. Our aim was to evaluate the specific changes that renal LECs undergo in HTN.

methodsWe performed single-cell RNA sequencing. Using the angiotensin II-induced and salt-sensitive mouse models of HTN, we isolated renal CD31+ and podoplanin+ cells.

resultsSequencing of these cells revealed three distinct cell types with unique expression profiles, including LECs. The number and transcriptional diversity of LECs increased in samples from mice with HTN, as demonstrated by 597 differentially expressed genes (p < 0.01), 274 significantly enriched pathways (p < 0.01), and 331 regulons with specific enrichment in HTN LECs. These changes demonstrate a profound inflammatory response in renal LECs in HTN, leading to an increase in genes and pathways associated with inflammation-driven growth and immune checkpoint activity in LECs.

conclusionThese results reinforce and help to further explain the benefits of renal LECs and lymphangiogenesis in HTN.

Indexed as

Disease Models, AnimalEndothelial CellsHypertensionInflammationKidneyAnimalsGene ExpressionLymphangiogenesisMiceGene expressionHypertensionInflammationKidneyLymphatics

Identifiers

PMID38972305
PMCPMC11345939

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.