ArticleAmerican journal of translational research2018
Role of Krüppel-like factor 4 in cigarette smoke-induced pulmonary vascular remodeling.
Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- The Role of Smoking in the Mechanisms of Development of Chronic Obstructive Pulmonary Disease and Atherosclerosis.International journal of molecular sciences · 2023Review
- MicroRNA miR-627-5p restrains pulmonary artery smooth muscle cell dysfunction by targeting MAP 2 K4 and PI3K/AKT signaling.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2022Article
- Advances in pathogenesis and treatment of essential hypertension.Frontiers in cardiovascular medicine · 2022Review
- TRB3 mediates vascular remodeling by activating the MAPK signaling pathway in hypoxic pulmonary hypertension.Respiratory research · 2021Article
- The preventive and therapeutic effects of AAV1-KLF4-shRNA in cigarette smoke-induced pulmonary hypertension.Journal of cellular and molecular medicine · 2021Article
- Article
- Role of RASEF hypermethylation in cigarette smoke-induced pulmonary arterial smooth muscle remodeling.Respiratory research · 2019Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pulmonary hypertension (PH) is characterized by excessive proliferation of pulmonary artery smooth muscle cells (PASMCs), leading to dysregulated vascular remodeling. Cigarette smoke (CS) is a common risk factor causing PH, and our previous study showed that CS extract (CSE) stimulated abnormal PASMC proliferation. However, the molecular mechanism remains unclear. In systemic circulation, vascular remodeling in some diseases is associated with upregulation of Krüppel-like factor 4 (KLF4), which stimulates the proliferation of vascular smooth muscle cells. We therefore hypothesized that upregulation of KLF4 may play a role in pulmonary vascular remodeling and the development of PH. Our results showed that KLF4 expression was increased significantly in remodeled pulmonary arteries from the rat smoking model of pulmonary vascular remodeling, compared with controls. In human PASMCs in vitro, KLF4 knockdown by gene silencing decreased proliferation and migration significantly. At the same time, it inhibited the CSE-induced increase of AKT phosphorylation. These results indicate that KLF4 contributes to CS-induced pulmonary vascular remodeling, and that KLF4 gene knockdown may be a useful therapeutic intervention for PH.
Indexed as
Identifiers
29511453PMC5835824W2980746648What OpenQuestion holds
Registered trials
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.