ArticleCellular and molecular life sciences : CMLS2024
N6-methyladenosine-driven miR-143/145-KLF4 circuit orchestrates the phenotypic switch of pulmonary artery smooth muscle cells.
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Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed.
- Secretory Carrier Membrane Protein 3 Knockdown Attenuates Hypoxic Pulmonary Hypertension Potentially Involving WW Domain-Containing E3 Ubiquitin Protein Ligase 1.Biochemical genetics · 2026Article
- mBiomolecules · 2026Review
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- Nanomaterials and exercise interventions: A synergistic approach for atherosclerosis therapy (Review).International journal of molecular medicine · 2026Review
- Advances in miRNA research: Unraveling the complexities of gene regulation.Animal models and experimental medicine · 2025Review
- miRNAs in Pulmonary Hypertension: Mechanistic Insights and Therapeutic Potential.Biomedicines · 2025Review
- Suv39h1 Regulates Phenotypic Modulation of Smooth Muscle Cells and Contributes to Vascular Injury by Repressing HIC1 Transcription.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- METTL14 promotes intimal hyperplasia through m6A-mediated control of vascular smooth muscle dedifferentiation genes.JCI insight · 2025Article
- Review
- miRNA regulatory networks as precision diagnostic and therapeutic targets in pulmonary arterial hypertension: from molecular cascades to clinical translation.American journal of cardiovascular disease · 2025Review
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Authors and funding
25 authors.
Kang Kang *Department of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.ORCID http://orcid.org/0000-0002-2080-2153
Chuannan Sun *Department of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Hui LiDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Xiaojia LiuDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Jingyuan DengDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Silei ChenDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, 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.
Jiahao ChenDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Xinyi LiuDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Jiahao KuangDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Jingjing XiangDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Jingqian ChengDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, 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.
Mujin LinDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Xingshi ZhangDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Chuzhi ZhanDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, China.
Sisi LiuDepartment of Biochemistry and Molecular Biology, Shenzhen University Medical School, Shenzhen, 518060, Guangdong, 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.
Cai LiangShenzhen 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.
Jinsheng ZhuState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, Guangdong, China.
Shuxin LiangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, Guangdong, China.
Haiyang TangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, Guangdong, 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 202201AY070001-224National 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-HX04Science and Technology Plan Projects of Tibet Autonomous Region JCYJ20210324120206017Shenzen Municipal and Hong Kong Joint Innovation Project SGDX20201103095404019Shenzhen stable support for general projects 8940317-0109Yunnan Provincial People's Hospital Cooperation Project 202201AY070001-224
Abstract
Pulmonary hypertension (PH) is characterized by vascular remodeling predominantly driven by a phenotypic switching in pulmonary artery smooth muscle cells (PASMCs). However, the underlying mechanisms for this phenotypic alteration remain incompletely understood. Here, we identified that RNA methyltransferase METTL3 is significantly elevated in the lungs of hypoxic PH (HPH) mice and rats, as well as in the pulmonary arteries (PAs) of HPH rats. Targeted deletion of Mettl3 in smooth muscle cells exacerbated hemodynamic consequences of hypoxia-induced PH and accelerated pulmonary vascular remodeling in vivo. Additionally, the absence of METTL3 markedly induced phenotypic switching in PASMCs in vitro. Mechanistically, METTL3 depletion attenuated m
Indexed as
AdenosineKruppel-Like Factor 4Kruppel-Like Transcription FactorsMethyltransferasesMicroRNAsMyocytes, Smooth MusclePulmonary ArteryAnimalsHumansHypertension, PulmonaryMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularPhenotypeRatsAdenosineKLF4 protein, humanKlf4 protein, mouseKlf4 protein, ratKruppel-Like Factor 4Kruppel-Like Transcription FactorsMethyltransferasesMettl3 protein, mouseMicroRNAsMIRN143 microRNA, mouseMIRN143 microRNA, ratMIRN145a microRNA, mouseMIRN145 microRNA, ratN-methyladenosineMethylationmicroRNANon-coding RNAPulmonary arterial hypertensionTranscription factor
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