ArticleExperimental and therapeutic medicine2019
PDCD4 expression in coronary atherosclerosis rat models and its mechanism.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- Programmed cell death protein 4 (PDCD4): a pleiotropic regulator in cardiovascular diseases.Journal of physiology and biochemistry · 2026Review
- Differential Pattern of Circulating MicroRNA Expression in Patients with Intracranial Atherosclerosis.Biomedicines · 2025Article
- PDCD4 promotes inflammation/fibrosis by activating the PPAR‑γ/NF‑κB pathway in mouse atrial myocytes.Molecular medicine reports · 2024Article
- Tripeptide Leu-Ser-Trp Regulates the Vascular Endothelial Cells Phenotype Switching by Mediating the Vascular Smooth Muscle Cells-Derived Small Extracellular Vesicles Packaging of miR-145.Molecules (Basel, Switzerland) · 2022Article
- WWP2 ameliorates oxidative stress and inflammation in atherosclerotic mice through regulation of PDCD4/HO-1 pathway.Acta biochimica et biophysica Sinica · 2022Article
- The mir-21 Inhibition Enhanced HUVEC Cellular Viability during Hypoxia-Reoxygenation Injury by Regulating PDCD4.Mediators of inflammation · 2022Article
- Association between fibrinogen-to-albumin ratio and the presence and severity of coronary artery disease in patients with acute coronary syndrome.BMC cardiovascular disorders · 2021Article
- Dysregulation of microRNA Modulatory Network in Abdominal Aortic Aneurysm.Journal of clinical medicine · 2020Article
- MicroRNA-532-5p protects against atherosclerosis through inhibiting vascular smooth muscle cell proliferation and migration.Cardiovascular diagnosis and therapy · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the expression of programmed cell death protein 4 (PDCD4) in rat models of coronary atherosclerosis (AS) and analyzed its role and mechanism. A total of 80 Wistar rats were selected and divided into the control group (n=40) and research group (n=40) according to the principle of similar body weight, of which coronary AS models were established in rats in the research group. PDCD4 expression in coronary artery tissues was detected using western blotting, and the expression of interleukin-6 (IL-6) and IL-8 in the coronary artery tissues were measured by means of reverse transcription-polymerase chain reaction (RT-PCR). The apoptotic rate of coronary artery smooth muscle cells was determined via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The relative expression of PDCD4 in coronary artery tissues in the research group was obviously higher than that in the control group, and the difference was statistically significant (t=6.121, P<0.01). In terms of the relative expression of messenger ribonucleic acid (mRNA) of IL-6 in the coronary artery tissues, the research group had a remarkably higher level than the control group, with a statistically significant difference (t=21.03, P<0.01). The difference in the relative expression of IL-8 mRNA between the research group and the control group was statistically significant, of which a much higher level was detected in the research group (t=19.96, P<0.01). The apoptotic rate of smooth muscle cells in the research group was increased notably compared with that in the control group, and the difference was statistically significant (t=5.985, P<0.01). PDCD4 may participate in the formation of coronary AS plaque, and its possible function in the process is to inhibit the proliferation of vascular smooth muscle cells and promote the upregulation of IL-6 and IL-8.
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