ArticleCellular & molecular biology letters2024
N6-methyladenosine modification of KLF2 may contribute to endothelial-to-mesenchymal transition in pulmonary hypertension.
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Article in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed.
- GLSP ameliorates monocrotaline-induced pulmonary arterial hypertension through inhibition of the PI3K/AKT and MAPK signaling pathways.Journal of molecular histology · 2026Article
- Hypoxic Pulmonary Hypertension: Molecular Mechanisms and Clinical Research Advances.International journal of molecular sciences · 2026Review
- A second-hit conceptual framework for pulmonary arterial hypertension in adult congenital heart disease: genetics, hemodynamics, and treat-and-repair.Frontiers in cardiovascular medicine · 2026Review
- Current Evidence on the Potential Role of EndothelialReviews in cardiovascular medicine · 2026Review
- The Role of Exosomes in Pulmonary Hypertension: Mechanisms and Therapeutic Potential.International journal of nanomedicine · 2026Review
- Flavonoids: Potential New Drug Candidates for Attenuating Vascular Remodeling in Pulmonary Hypertension.International journal of molecular sciences · 2025Review
- The Emerging Role of METTL3 in Lung Diseases.International journal of molecular sciences · 2025Review
- Research advances in epigenetic modifications and post-translational modifications in endothelial-mesenchymal transition.Epigenetics & chromatin · 2025Review
- NAT10 induces N4-acetylcytidine modification of AdipoR1-mediated mitochondrial biogenesis against endothelial-to-mesenchymal transition in hypertension.Molecular medicine (Cambridge, Mass.) · 2025Article
- Rewriting the vascular script: epigenetic modifiers as scribes of metabolic reprogramming in pulmonary hypertension.Journal of molecular medicine (Berlin, Germany) · 2025Review
- eNAMPT/TLR4 signaling drives PAH cellular phenotypic switching and lung vascular remodeling.Cell communication and signaling : CCS · 2025Article
- Follicle-stimulating hormone promotes EndMT in endothelial cells by upregulating ALKBH5 expression.Cellular & molecular biology letters · 2025Article
- Review
- High Shear Stress Reduces ERG Causing Endothelial-Mesenchymal Transition and Pulmonary Arterial Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Mechanism of Tetrandrine in Ameliorating Hypoxic Pulmonary Hypertension Vascular Remodeling through Transcriptomics and Metabolomics.Current drug metabolism · 2025Article
- Mechanism of action and potential therapeutic targets of TGF-β-related signaling pathway and its downstream miRNA expression in pulmonary arterial hypertension.Frontiers in pharmacology · 2025Review
- Krüppel-like factor 2 is an endoprotective transcription factor in diabetic kidney disease.American journal of physiology. Cell physiology · 2024Review
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Authors and funding
19 authors.
Kang Kang *Department of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.ORCID http://orcid.org/0000-0002-2080-2153
Jingjing Xiang *Department of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Xingshi Zhang *Department of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Yuting XieDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Mengting ZhouDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Le ZengShenzhen Key Laboratory of Microbial Genetic Engineering, Vascular Disease Research Center, College of Life Sciences and Oceanography, Guangdong Provincial Key Laboratory of Regional Immunity and Disease, Carson International Cancer Center, School of Medicine, Shenzhen University, Shenzhen, 518060, China.
Junhao ZhuangDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Jiahao KuangDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Yuanyuan LinDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Bozhe HuDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Qianmin XiongDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Qing YinDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, People's Republic of China.
Qiang SuShenzhen Key Laboratory of Microbial Genetic Engineering, Vascular Disease Research Center, College of Life Sciences and Oceanography, Guangdong Provincial Key Laboratory of Regional Immunity and Disease, Carson International Cancer Center, School of Medicine, Shenzhen University, Shenzhen, 518060, China.
Xiaoyun LiaoShenzhen Key Laboratory of Microbial Genetic Engineering, Vascular Disease Research Center, College of Life Sciences and Oceanography, Guangdong Provincial Key Laboratory of Regional Immunity and Disease, Carson International Cancer Center, School of Medicine, Shenzhen University, Shenzhen, 518060, China.
Jun WangShenzhen Key Laboratory of Microbial Genetic Engineering, Vascular Disease Research Center, College of Life Sciences and Oceanography, Guangdong Provincial Key Laboratory of Regional Immunity and Disease, Carson International Cancer Center, School of Medicine, Shenzhen University, Shenzhen, 518060, China.
Yanqin NiuShenzhen Key Laboratory of Microbial Genetic Engineering, Vascular Disease Research Center, College of Life Sciences and Oceanography, Guangdong Provincial Key Laboratory of Regional Immunity and Disease, Carson International Cancer Center, School of Medicine, Shenzhen University, Shenzhen, 518060, China.
Cuilian LiuShenzhen Key Laboratory of Microbial Genetic Engineering, Vascular Disease Research Center, College of Life Sciences and Oceanography, Guangdong Provincial Key Laboratory of Regional Immunity and Disease, Carson International Cancer Center, School of Medicine, Shenzhen University, Shenzhen, 518060, China.
Jinglin TianShenzhen Key Laboratory of Microbial Genetic Engineering, Vascular Disease Research Center, College of Life Sciences and Oceanography, Guangdong Provincial Key Laboratory of Regional Immunity and Disease, Carson International Cancer Center, School of Medicine, Shenzhen University, Shenzhen, 518060, China.
Deming GouShenzhen Key Laboratory of Microbial Genetic Engineering, Vascular Disease Research Center, College of Life Sciences and Oceanography, Guangdong Provincial Key Laboratory of Regional Immunity and Disease, Carson International Cancer Center, School of Medicine, Shenzhen University, Shenzhen, 518060, China. dmgou@szu.edu.cn.ORCID http://orcid.org/0000-0002-3312-841X
Funding
Joint Project of Basic Research and Applied Basic Research in Yunnan Province 202201AY070001-224Key Basic Research Projects of Shenzhen JCYJ20210324120206017National Natural Science Foundation of China 81970053National Natural Science Foundation of China 82170070National Natural Science Foundation of China 82241022National Natural Science Foundation of China 82270054National Natural Science Foundation of China 82300076National Natural Science Foundation of China 82370065National Natural Science Foundation of China 89202586Open Project of Respiratory Disease Clinical Medical Center of Yunnan Province 2022LCZXKF-HX03Open Project of Respiratory Disease Clinical Medical Center of Yunnan Province 2022LCZXKF-HX04Shenzen Municipal and Hong Kong Joint Innovation Project SGDX20201103095404019Shenzhen Stable Support for General Projects 8940317-0109
Abstract
backgroundPulmonary hypertension (PH) is a progressive disease characterized by pulmonary vascular remodeling. Increasing evidence indicates that endothelial-to-mesenchymal transition (EndMT) in pulmonary artery endothelial cells (PAECs) is a pivotal trigger initiating this remodeling. However, the regulatory mechanisms underlying EndMT in PH are still not fully understood.
methodsCytokine-induced hPAECs were assessed using RNA methylation quantification, qRT-PCR, and western blotting to determine the involvement of N6-methyladenosine (m
resultsThe global levels of m
conclusionsOur findings unveil a novel METTL3/KLF2 pathway critical for protecting hPAECs against EndMT, highlighting a promising avenue for therapeutic investigation in PH.
Indexed as
AdenosineEndothelial CellsEpithelial-Mesenchymal TransitionHypertension, PulmonaryKruppel-Like Transcription FactorsMethyltransferasesAnimalsCadherinsCells, CulturedHumansMethylationMiceMice, Inbred C57BLPulmonary ArteryVascular RemodelingAdenosineCadherinsKLF2 protein, humanKruppel-Like Transcription FactorsMethyltransferasesMETTL3 protein, humanMettl3 protein, mouseN-methyladenosineEpigeneticsEpithelial-mesenchymal transitionMethylationPulmonary arterial hypertensionTranscription factor
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