Evidence map›Paper›PMID 40533529›Full record

ArticleHypertension research : official journal of the Japanese Society of Hypertension2025

Oxidized LDL enhances Gq signaling and aldosterone production by angiotensin II via the AT1-LOX-1 receptor complex in adrenal cells.

Jittoku Ihara, Yibin Huang, Yoichi Takami, Yu Guo, Toshimasa Takahashi, Akemi Kakino, Yoichi Nozato, Cheng Wang, Ziwei Wang, Weidong Liu and 7 more

Abstract read
In one paragraph

Article in Hypertension research : official journal of the Japanese Society of Hypertension, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Be careful of hidden friends.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Jittoku IharaDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Yibin HuangDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Yoichi TakamiDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan. takami@geriat.med.osaka-u.ac.jp.
Yu GuoDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Toshimasa TakahashiDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Akemi KakinoDepartment of Molecular Pathophysiology, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan.
Yoichi NozatoDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Cheng WangDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Ziwei WangDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Weidong LiuDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Nanxiang YinDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Ryoichi OharaDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Akitoshi HaraDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Hikari TakeshitaDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Hiromi RakugiDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Tatsuya SawamuraDepartment of Molecular Pathophysiology, Shinshu University Graduate School of Medicine, Matsumoto, Nagano, Japan.
Koichi YamamotoDepartment of Geriatric and General Medicine, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that oxidized low-density lipoprotein (oxLDL) activates the angiotensin II (AII) type 1 receptor (AT1) through the lectin-like oxLDL receptor (LOX-1)-AT1 complex. While oxLDL alone does not activate G protein αq (Gq), its simultaneous binding with AII alters AT1 structure, enhancing Gq activation. We investigated this interaction's effect on aldosterone production in adrenal glands. Human adrenal cells (H295R) were treated with vehicle, oxLDL, AII, or a combination of oxLDL and AII. Gq signaling was assessed using inositol monophosphate (IP1) assays, Ca influx using Fura2, and aldosterone synthesis gene expression using qRT-PCR. Wild-type (WT) and LOX-1 knockout (KO) mice were fed a normal diet (ND) or high-fat diet (HFD) in vivo to elevate oxLDL levels, followed by subcutaneous AII or saline infusion for 4 weeks (long-term) or 3 days (short-term). In H295R cells, oxLDL alone did not induce IP1 production; however, AII-induced IP1 and Ca influx were enhanced by oxLDL. These effects were abolished by LOX-1 siRNA. Co-administration of oxLDL and AII upregulated aldosterone synthesis genes, such as CYP11B2; this effect was suppressed by a Gq inhibitor. In vivo, long-term AII and HFD administration increased adrenal CYP11B2 expression but not serum aldosterone levels. Conversely, short-term AII and oxLDL administration elevated serum aldosterone levels, but not CYP11B2 expression. These effects were absent in LOX-1 KO mice. Blood pressure was unaffected by HFD or oxLDL in both models. In conclusion, OxLDL enhances AII-induced aldosterone production in adrenal glands through LOX-1-AT1 interaction, although its impact on blood pressure regulation remains unclear. Oxidized LDL enhances Gq signaling and aldosterone production by angiotensin II via the AT1-LOX-1 receptor complex in adrenal cells. LOX-1 amplifies angiotensin II-induced aldosterone synthesis by modulating AT1 receptor signaling in adrenal glands. Co-stimulation with oxLDL enhances Gq activation via LOX-1-AT1 interaction, potentially through AT1 unique conformational changes. These findings underscore the interplay between dyslipidemia and RAAS in promoting hypertension and cardiovascular diseases.

Indexed as

Adrenal GlandsAldosteroneAngiotensin IIGTP-Binding Protein alpha Subunits, Gq-G11Lipoproteins, LDLReceptor, Angiotensin, Type 1Scavenger Receptors, Class EAnimalsHumansMaleMiceMice, KnockoutSignal TransductionAldosteroneAngiotensin IIGTP-Binding Protein alpha Subunits, Gq-G11Lipoproteins, LDLoxidized low density lipoproteinReceptor, Angiotensin, Type 1Scavenger Receptors, Class EAdrenal cellsAldosteroneAngiotensin IIAT1-LOX-1 receptor complexOxidized LDL

Identifiers

PMID40533529
PMCPMC12411259

What Socratic holds

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LicenceCC BY
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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 Socratic graph.