Underlying image data supporting Fig 2A.

NIAID Data Ecosystem2026-05-02 收录

肺动脉高压分子机制

端粒酶逆转录酶正反馈环路

数据链接：

https://figshare.com/articles/dataset/Underlying_image_data_supporting_Fig_2A_/26523286 数据链接链接失效反馈

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Correction: Positive Feedback-Loop of Telomerase Reverse Transcriptase and 15-Lipoxygenase-2 Promotes Pulmonary Hypertension

创建时间：

2024-08-08

E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension. E2F1 mediates SOX17 Deficiency-Induced Pulmonary Hypertension

肺动脉高压分子机制

内皮细胞转录调控

SRY-Box Transcription Factor 17 (SOX17) enhancers variants and mutations are found in patients with pulmonary arterial hypertension (PAH). In human PAH pulmonary microvascular endothelial cells (HPMVE

NIAID Data Ecosystem70

MOESM1 of Transcriptome-wide map of m6A circRNAs identified in a rat model of hypoxia mediated pulmonary hypertension

RNA表观遗传学

肺动脉高压分子机制

Additional file 1: Data S1. Differentially expressed m6A abundance in circRNAs.

Figshare2020-01-14 更新50

Data_Sheet_1_Weighted gene co-expression network analysis identifies dysregulated B-cell receptor signaling pathway and novel genes in pulmonary arterial hypertension.PDF

肺动脉高压分子机制

受体信号通路

BackgroundPulmonary arterial hypertension (PAH) is a devastating cardio-pulmonary vascular disease in which chronic elevated pulmonary arterial pressure and pulmonary vascular remodeling lead to right

NIAID Data Ecosystem10

PPARγ Ligands Attenuate Hypoxia-Induced Proliferation in Human Pulmonary Artery Smooth Muscle Cells through Modulation of MicroRNA-21

肺动脉高压分子机制

MicroRNA调控

Pulmonary hypertension (PH) is a progressive and often fatal disorder whose pathogenesis involves pulmonary artery smooth muscle cell (PASMC) proliferation. Although modern PH therapies have significa

NIAID Data Ecosystem60

E-cigarettes induce dysregulation of autophagy leading to endothelial dysfunction in pulmonary arterial hypertension. E-cigarettes induce dysregulation of autophagy leading to endothelial dysfunction in pulmonary arterial hypertension

电子烟毒性

肺动脉高压分子机制

To investigate whether differential susceptibility exists between healthy and PAH patients to e-cig exposure and the molecular mechanisms, human iPSC lines from two healthy volunteers and two FPAH pat

NIAID Data Ecosystem50

Underlying image data supporting Fig 2A.

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