Mechanism of isosorbide dinitrate combined with exercise training rehabilitation to mobilize endothelial progenitor cells in patients with coronary heart disease

Abstract

Ruozhu Dai, Huilin Zhuo, Yangchun Chen, Kelian Zhang, Yongda Dong, Chengbo Chen and Wei Wang. Mechanism of isosorbide dinitrate combined with exercise training rehabilitation to mobilize endothelial progenitor cells in patients with coronary heart disease. Bioengineered. 2021 Nov. doi: 10.1080/21655979.2021.2000258. Since publication, significant concerns have been raised about the compliance with ethical policies for human research and the integrity of the data reported in the article. When approached for an explanation, the authors provided some original data but were not able to provide all the necessary supporting information. As verifying the validity of published work is core to the scholarly record’s integrity, we are retracting the article. All authors listed in this publication have been informed. We have been informed in our decision-making by our editorial policies and the COPE guidelines. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as ‘Retracted.’

Cardiopulmonary Exercise Performance and Endothelial Function in Convalescent COVID-19 Patients

“…Among them, renin–angiotensin system (RAS) inhibitors and statins, which have shown to improve endothelial function in other clinical settings [ 40 ], have been tested in large observational studies and randomized trials with contrasting results in COVID-19 [ 41 , 42 , 43 ]. The positive impact of exercise on endothelial function has been known for a long time both in healthy subjects and in different clinical settings (e.g., chronic obstructive pulmonary disease, heart failure) [ 44 , 45 , 46 , 47 ]. A number of mechanisms have been proposed to explain the beneficial effects of exercise-based strategies on endothelial function, including mobilization of endothelial progenitor cells, upregulation of superoxide dismutase, and reduced uncoupling with increased phosphorylation of endothelial NO synthase [ 48 ].…”

Restenosis after Coronary Stent Implantation: Cellular Mechanisms and Potential of Endothelial Progenitor Cells (A Short Guide for the Interventional Cardiologist)

“…It is believed that a dysfunction of PCs may at least partially explain the association between patient characteristics such as age, diabetes mellitus, hyperlipidemia and renal impairment and the risk of restenosis [61]. On the other side, the administration of nitric oxide donors such as organic nitrates and/or physical exercise may actually increase the counts of CD133+, CD34+ and vascular endothelial growth factor receptor positive cells, as well as their proliferation activity, adhesion and migration ability in patients with coronary artery disease [62]. Finally, the impact of various other pharmacological interventions on the number and function of PCs has also been shown, including statins, angiotensin converting enzyme inhibitors, angiotensin blockers, beta-blockers and clopidogrel [63,64].…”