Evidence map›Paper›PMID 42086537›Full record

ArticleCell death discovery2026

YWHAZ-mediated metabolic reprogramming via HIF1A/LDHA signaling promotes pulmonary arterial remodelling.

Zhong-Yuan Meng, Chuang-Hong Lu, Juan Liao, Sen-Hu Tang, Jing Li, Xiao-Li Ma, Yue Qin, Chao-Yong Zhang, Yao-Shi Hu, De-Xin Chen and 4 more

Abstract read
In one paragraph

Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

14 authors.

Zhong-Yuan Meng *Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Chuang-Hong Lu *Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Juan Liao *Ultrasound Department, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Sen-Hu Tang *Department of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Jing LiDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Xiao-Li MaDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Yue QinGuangxi Key Laboratory of Precision Medicine in Cardio-cerebrovascular Diseases Control and Prevention, Guangxi Clinical Research Center for Cardio-cerebrovascular Diseases, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Chao-Yong ZhangDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Yao-Shi HuDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
De-Xin ChenDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Xing ChenUltrasound Department, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China.
Yan DengUltrasound Department, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China. 190662044@qq.com.
Feng HuangDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China. huangfeng@sr.gxmu.edu.cn.
Zhi-Yu ZengDepartment of Cardiology, The First Affiliated Hospital of Guangxi Medical University, No.6 Shuangyong Road, Nanning, Guangxi, 530021, China. zengzhiyu@gxmu.edu.cn.ORCID http://orcid.org/0000-0002-7383-2700

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia-related pulmonary arterial hypertension (PAH) remains poorly managed by current therapies. Metabolic dysregulation, particularly glycolysis, plays a key role in PAH pathogenesis. This study investigated YWHAZ's role in PAH using hypoxia-induced pulmonary arterial endothelial cells (PAECs) and a hypoxia/SU5416-induced PAH rat model. Silencing YWHAZ inhibited PAEC proliferation, migration, and glycolysis, while improving right ventricular function and reducing pulmonary vascular remodeling. Mechanistically, YWHAZ stabilized HIF-1α, which transcriptionally activated LDHA, a critical glycolytic enzyme. HIF-1α agonist treatment reversed YWHAZ silencing effects, confirming the YWHAZ/HIF-1α/LDHA axis. These findings highlight YWHAZ as a potential therapeutic target for metabolic intervention in PAH.

Identifiers

PMID42086537
PMCPMC13287781

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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.