36 Papers
68 Citations
Cui Ma is an academic researcher from Harbin Medical University. The author has contributed to research in topics: Hypoxia (medical) & Pulmonary hypertension. The author has an hindex of 15, co-authored 36 publications.
Chat about Author
Papers
Circular RNA Calm4 Regulates Hypoxia-Induced Pulmonary Arterial Smooth Muscle Cells Pyroptosis via the Circ-Calm4/miR-124-3p/PDCD6 Axis.
Yuan Jiang,Huiyu Liu,Hang Yu,Yang Zhou,Junting Zhang,Wei Xin,Yiying Li,Siyu He,Cui Ma,Xiaodong Zheng,Lixin Zhang,Xijuan Zhao,Bingxiang Wu,Chun Jiang,Daling Zhu +14 more
TL;DR: In this article, a specific circular RNA known as circ-calm4 was found to act as a competitive endogenous RNA to regulate miR-124-3p in pulmonary arterial smooth muscle cell pyroptosis.
82
Circ-calm4 Serves as an miR-337-3p Sponge to Regulate Myo10 (Myosin 10) and Promote Pulmonary Artery Smooth Muscle Proliferation.
Junting Zhang,Yiying Li,Jing Qi,Xiufeng Yu,Huanhuan Ren,Xijuan Zhao,Wei Xin,Siyu He,Xiaodong Zheng,Cui Ma,Lixin Zhang,Bingxiang Wu,Daling Zhu +12 more
TL;DR: The results suggested that the circ-calm4/miR-337-3p/Myo10 signal transduction axis modulated the proliferation of pulmonary artery smooth muscle cells at the molecular level, thus establishing potential targets for the early diagnosis and treatment of pulmonary hypertension.
74
Long noncoding RNA Hoxaas3 contributes to hypoxia-induced pulmonary artery smooth muscle cell proliferation
Hongyue Zhang,Ying Liu,Lixin Yan,Siqi Wang,Min Zhang,Cui Ma,Xiaodong Zheng,He Chen,Daling Zhu +8 more
TL;DR: This study defined the role and mechanism of action of Hoxaas3 in the regulation of cell proliferation in PH, which should facilitate the development of new therapeutic strategies for the treatment of this disease.
54
The role of PDGF-B/TGF-β1/neprilysin network in regulating endothelial-to-mesenchymal transition in pulmonary artery remodeling.
Shasha Song,Min Zhang,Zhi Yi,Hongyue Zhang,Tingting Shen,Xiufeng Yu,Chen Zhang,Xiaodong Zheng,Lei Yu,Cui Ma,Yang Liu,Daling Zhu +11 more
TL;DR: The results identify a novel mechanism to reveal the formation of EndoMT in PAH, and imply that imatinib may serve as a new therapeutic approach for treatment of the third cardiovascular disease.
54
Hyperoxia Causes Mitochondrial Fragmentation in Pulmonary Endothelial Cells by Increasing Expression of Pro-Fission Proteins.
Cui Ma,Andreas M. Beyer,Matthew J. Durand,Anne V. Clough,Daling Zhu,Laura E Norwood Toro,Maia Terashvili,Johnathan D. Ebben,R. Blake Hill,Said H. Audi,Meetha Medhora,Elizabeth R. Jacobs +11 more
TL;DR: Because hyperoxia evoked mt-fragmentation, cell survival and transwell resistance are prevented by ENDO III and mito-TEMPOL and Drp-1 silencing, and these data linkhyperoxia-induced mt-DNA damage, Drp (dynamin-related protein 1) expression, mt- FRGmentation, and PEC dysfunction.