Evidence map›Paper›PMID 40362300›Full record

ArticleInternational journal of molecular sciences2025

Role of LMCD1 in the Long-Term Effects of Angiotensin II in Vascular Smooth Muscle Cells.

Janka Borbála Gém, Kinga Bernadett Kovács, Szilvia Barsi, Saba Hadadnejadtehrani, Amir Damouni, Gábor Turu, András Dávid Tóth, Péter Várnai, László Hunyady, András Balla

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 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. 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

10 authors.

Janka Borbála GémDepartment of Physiology, Faculty of Medicine, Semmelweis University, Tűzoltó utca 37-47, 1094 Budapest, Hungary.
Kinga Bernadett KovácsDepartment of Physiology, Faculty of Medicine, Semmelweis University, Tűzoltó utca 37-47, 1094 Budapest, Hungary.
Szilvia BarsiDepartment of Physiology, Faculty of Medicine, Semmelweis University, Tűzoltó utca 37-47, 1094 Budapest, Hungary.ORCID 0000-0002-8779-2383
Saba HadadnejadtehraniDepartment of Physiology, Faculty of Medicine, Semmelweis University, Tűzoltó utca 37-47, 1094 Budapest, Hungary.
Amir DamouniDepartment of Physiology, Faculty of Medicine, Semmelweis University, Tűzoltó utca 37-47, 1094 Budapest, Hungary.ORCID 0009-0008-9385-2419
Gábor TuruDepartment of Physiology, Faculty of Medicine, Semmelweis University, Tűzoltó utca 37-47, 1094 Budapest, Hungary.
András Dávid TóthInstitute of Molecular Life Sciences, Centre of Excellence of the Hungarian Academy of Sciences, HUN-REN-SU Research Centre of Natural Sciences, Magyar tudósok körútja 2, 1117 Budapest, Hungary.ORCID 0000-0003-2746-9370
Péter VárnaiDepartment of Physiology, Faculty of Medicine, Semmelweis University, Tűzoltó utca 37-47, 1094 Budapest, Hungary.ORCID 0000-0002-7777-806X
László HunyadyDepartment of Physiology, Faculty of Medicine, Semmelweis University, Tűzoltó utca 37-47, 1094 Budapest, Hungary.ORCID 0000-0002-8438-7251
András BallaDepartment of Physiology, Faculty of Medicine, Semmelweis University, Tűzoltó utca 37-47, 1094 Budapest, Hungary.

Funding

Hungarian National Research, Development and Innovation Fund K134357Hungarian National Research, Development and Innovation Fund NKFI K139231Semmelweis University STIA-OTKA
6 · The paper itself

Abstract

Excessive activity of the hormone angiotensin II (AngII) is known to contribute to the pathogenesis of multiple cardiovascular diseases, including atherosclerosis, vascular remodeling, and hypertension, primarily through inducing gene expression changes. In this study, we identified LMCD1 (LIM and cysteine-rich domains 1, also known as Dyxin), primarily recognized as a transcription co-factor involved in various oncogenic processes, cardiac hypertrophy, and vascular remodeling, as a potential key factor in AngII-mediated effects in vascular smooth muscle cells (VSMCs). We demonstrated that AngII upregulates

Indexed as

Angiotensin IILIM Domain ProteinsMuscle, Smooth, VascularMyocytes, Smooth MuscleAnimalsCalcium SignalingCell MovementCell ProliferationCells, CulturedMaleRatsRats, Sprague-DawleyReceptor, Angiotensin, Type 1Vascular RemodelingAngiotensin IILIM Domain ProteinsReceptor, Angiotensin, Type 1Angiotensin II (AngII)LIM and cysteine-rich domains 1 (LMCD1)mitogen-activated protein kinase (MAPK)type 1 angiotensin receptor (AT1-R)vascular smooth muscle cell (VSMC)

Identifiers

PMID40362300
PMCPMC12071511

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.