Evidence map›Paper›PMID 37034342›Full record

ArticleFrontiers in cardiovascular medicine2023

Cardiomyocyte-specific deletion of TLR4 attenuates angiotensin II-induced hypertension and cardiac remodeling.

Drew Theobald, Anand R Nair, Srinivas Sriramula, Joseph Francis

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cardiovascular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 12 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Cardiomyocytes regulate Inflammation in the failing heart.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. pH-sensing GPR68 inhibits vascular smooth muscle cell proliferation through Rap1A.American journal of physiology. Heart and circulatory physiology · 2024
    Article
  9. Article
  10. 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 2 institutions in 1 country.

Drew TheobaldDepartment of Pharmacology and Toxicology, Brody School of Medicine at East Carolina University, Greenville, NC, United States.
Anand R NairComparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, United States.
Srinivas SriramulaDepartment of Pharmacology and Toxicology, Brody School of Medicine at East Carolina University, Greenville, NC, United States.
Joseph FrancisComparative Biomedical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, LA, United States.
East Carolina University · USLouisiana State University · US

Funding

Mechanistic Insights to A Translatable Therapy for Acute Reperfused Hemorrhagic Myocardial InfarctionsR01HL147133 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI DHARMAKUMAR, ROHAN, FRANCIS, JOSEPH · 2020 to 2023
$3.2M
Neuroimmune Mechanisms of Kinin B1 Receptor in HypertensionR01HL153115 · NHLBI · EAST CAROLINA UNIVERSITY · PI SRIRAMULA, SRINIVAS · 2020 to 2024
$1.8M
NHLBI NIH HHS R01 HL147133NHLBI NIH HHS R01 HL153115
6 · The paper itself

Abstract

Toll-like receptor 4 (TLR4) is an integral factor in the initiation of the innate immune response and plays an important role in cardiovascular diseases such as hypertension and myocardial infarction. Previous studies from our lab demonstrated that central TLR4 blockade reduced cardiac TLR4 expression, attenuated hypertension, and improved cardiac function. However, the contribution of cardiac specific TLR4 to the development of hypertension and cardiac remodeling is unknown. Therefore, we hypothesized that cardiomyocyte specific knockdown of TLR4 would have beneficial effects on hypertension, cardiac hypertrophy, and remodeling. To test this hypothesis, cardiomyocyte-specific TLR4 knockdown (cTLR4KO) mice were generated by crossing floxed TLR4 mice with Myh6-Cre mice, and subjected to angiotensin II (Ang II, 1 µg/kg/min or vehicle for 14 days) hypertension model. Blood pressure measurements using radio telemetry revealed no differences in baseline mean arterial pressure between control littermates and cTLR4KO mice (103 ± 2 vs. 105 ± 3 mmHg,

Indexed as

angiotensin IIcardiac hypertrophyhypertensioninflammationTLR4

Identifiers

PMID37034342
PMCPMC10079917
OpenAlexW4360869905

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.