Evidence map›Paper›PMID 40088465›Full record

ArticleCardiovascular research2025

Protective functions of liver X receptor α on calcified aortic valve: involvement of regulating endoplasmic reticulum-mediated osteogenic differentiation.

Lishan Zeng, Xin Chen, Kai Kang, Yifei Lin, Zhongxing Zhou, Shuaijie Chen, Chunkai Huang, Qingqing Lin, Hongzhuang Wang, Longqing Chen and 5 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. Hypertensive mt. tRNARedox biology · 2026
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Lishan ZengCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Xin ChenCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Kai KangCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Yifei LinCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Zhongxing ZhouCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Shuaijie ChenCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Chunkai HuangCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Qingqing LinEchocardiological Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou 350005, China.
Hongzhuang WangCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Longqing ChenCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Liangliang YanCardiac Surgery Department, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.
HanFan QiuCardiac Surgery Department, The First Affiliated Hospital, Fujian Medical University, Fuzhou 350005, China.
Jinxiu LinCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.
Xiaoyan LinEchocardiological Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou 350005, China.
Dajun ChaiCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Key Laboratory of Metabolic Heart Disease in Fujian Province, Clinical Research Centre of Metabolic Cardiovascular Disease in Fujian Province, 20 Chazhong Road, Fuzhou 350005, China.ORCID 0000-0001-9477-9956

Funding

Fund for Young and Middle-aged Experts with Outstanding Contributions to Health in Fujian Province 2021ZQNZD005Joint Funds for the Innovation of Science and Technology, Fujian Province 2021Y9142University-Industry Research Joint Innovation Project of Science and Technology, Fujian Province 2020Y4016
6 · The paper itself

Abstract

aimsEffective therapeutic drugs for calcific aortic valve disease (CAVD) are lacking, although its incidence has been increasing over the past decade and is predicted to continue rising in the future. This study aimed to explore the role and potential mechanisms of liver X receptor α (LXRα) in CAVD, which offers a promising approach for treating CAVD. METHODS AND

resultsOsteogenic stimulation was performed following which a substantial downregulation of LXRα was observed in human calcific aortic valves and valvular interstitial cells. Further functional investigations revealed that silencing LXRα exacerbated calcification both in vitro and in vivo. We showed that LXRα suppressed the protein kinase R-like endoplasmic reticulum kinase/eukaryotic initiation factor 2/activating transcription factor 4 pathway, which controls endoplasmic reticulum stress (ERS) and promotes osteogenic differentiation, thereby slowing the course of CAVD.

conclusionOur research offers fresh perspectives on how LXRα controls the pathophysiology of CAVD via regulating ERS. The findings suggest that targeting LXRα is a potential treatment strategy for treating aortic valve calcification.

Indexed as

Aortic ValveAortic Valve StenosisCalcinosisCell DifferentiationEndoplasmic ReticulumEndoplasmic Reticulum StressLiver X ReceptorsOsteogenesisAnimalsCells, CulturedDisease Models, AnimaleIF-2 KinaseHumansMaleMice, Inbred C57BLSignal TransductioneIF-2 KinaseLiver X ReceptorsNR1H3 protein, humanNr1h3 protein, mouseCalcific aortic valve diseaseEndoplasmic reticulum stressLiver X receptor αValvular interstitial cells

Identifiers

PMID40088465
PMCPMC12160815

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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.