Evidence map›Paper›PMID 39021353›Full record

ArticleCell proliferation2024

Lipocalin-2 induced LDHA expression promotes vascular remodelling in pulmonary hypertension.

Guoliang Wang, Shenghua Liu, Xiaohui Kong, Hong Jiao, Feng Tong, Zhangke Guo, Meng Zhang, Xiaoxing Guan, Na Ren, Wanzhen Li and 2 more

Abstract read
In one paragraph

Article in Cell proliferation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
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  4. Review
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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

12 authors.

Guoliang WangDepartment of Tumor and Immunology, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.ORCID https://orcid.org/0000-0002-9191-6166
Shenghua LiuState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Xiaohui KongDepartment of Tumor and Immunology, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Hong JiaoDepartment of Tumor and Immunology, Beijing Pediatric Research Institute, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Feng TongDepartment of Cardiac Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Zhangke GuoDepartment of Cardiac Surgery, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Meng ZhangDepartment of Pathology, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Xiaoxing GuanDepartment of Pathology, Beijing Children's Hospital, Capital Medical University, National Center for Children's Health, Beijing, China.
Na RenDepartment of Clinical Laboratory Center, Beijing Children's Hospital, Capital Medical University, Beijing, China.
Wanzhen LiDepartment of Lipidomics Experimental Platform, State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Lihua QiDepartment of Human Anatomy, Histology and Embryology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yingjie WeiState Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.

Funding

the CAMS Innovation Fund for the Medical Sciences 2016-I2M-1-015the National Natural Science Foundation of China 81470424the Natural Science Cultivation Fund of Capital Medical University, china PYZ2017104
6 · The paper itself

Abstract

Aerobic glycolysis is involved in the pathogenesis of pulmonary hypertension (PH). The mechanisms by which glycolysis is increased and how it contributes to pulmonary vascular remodelling are not yet fully understood. In this study, we demonstrated that elevated lipocalin-2 (LCN2) in PH significantly enhances aerobic glycolysis in human pulmonary artery smooth muscle cells (PASMCs) by up-regulating LDHA expression. Knockout of Lcn2 or having heterozygous LDHA deficiency in mice significantly inhibits the progression of hypoxic PH. Our study reveals that LCN2 stimulates LDHA expression by activating Akt-HIF-1α signalling pathway. Inhibition of Akt or HIF-1α reduces LDHA expression and proliferation of PASMCs. Both Akt and HIF-1α play critical roles in the development of PH and are suppressed in the pulmonary vessels of hypoxic PH mice lacking LCN2. These findings shed light on the LCN2-Akt-HIF1α-LDHA axis in aerobic glycolysis in PH.

Indexed as

GlycolysisHypertension, PulmonaryHypoxia-Inducible Factor 1, alpha SubunitLipocalin-2Proto-Oncogene Proteins c-aktSignal TransductionVascular RemodelingAnimalsCell ProliferationCells, CulturedHumansLactate Dehydrogenase 5L-Lactate DehydrogenaseMaleMiceMice, Inbred C57BLHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitLactate Dehydrogenase 5LCN2 protein, humanLcn2 protein, mouseLDHA protein, humanLipocalin-2L-Lactate DehydrogenaseProto-Oncogene Proteins c-akt

Identifiers

PMID39021353
PMCPMC11628741

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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 OpenQuestion graph.