Exosomes secreted by FNDC5-BMMSCs protect myocardial infarction by anti-inflammation and macrophage polarization via NF-κB signaling pathway and Nrf2/HO-1 axis.

Background: Exosomes are considered a substitute for stem cell-based therapy for myocardial infarction (MI). FNDC5, a transmembrane protein located in the cytoplasm, plays a crucial role in inflammation diseases and MI repair. Furthermore, our previous study found that FNDC5 pre-conditioning bone marrow-derived mesenchymal stem cells (BMMSCs) could secrete more exosomes, but little was known on MI repair.

Irisin ameliorates high glucose-induced cardiomyocytes injury via AMPK/mTOR signal pathway.

High glucose (HG)-induced cardiomyocytes (CMs) injury is a leading cause of diabetic cardiomyopathy with little treatment options. Irisin, a new myokine, which is cleaved from its precursor fibronectin type III domain-containing protein 5 (FNDC5), has aroused great attention as an essential cardioprotective factor and glucose metabolism regulator but little was known on diabetic cardiomyopathy yet. Here, we aim to clarify the role of irisin in the HG-induced CMs injury.

β-arrestin1 inhibits hypoxic injury-induced autophagy in human pulmonary artery endothelial cells via the Akt/mTOR signaling pathway.

Autophagy has been greatly implicated in injured endothelial cells during pulmonary arterial hypertension (PAH). β-arrestin1, a multifunctional cytoplasmic protein, has attracted considerable attention as an essential protective factor in PAH. However, its role in autophagy of injured pulmonary arterial endothelial cells (PAECs) remains to be determined.

[Corrigendum] CENPE promotes lung adenocarcinoma proliferation and is directly regulated by FOXM1.

Subsequently to the publication of this article, the authors have realized that the order of the corresponding authors in the author list should have been reversed: Wenshu Chai was listed as the penultimate author on the paper, whereas Xianbao Shi should have been featured before Wenshu Chai. Therefore, the authors and affiliations for this paper should have appeared as follows: LINA SHAN1, MINJIE ZHAO1, YA LU1, HONGJUAN NING1, SHUMAN YANG2, YONGGUI SONG3, XIANBAO SHI1 and WENSHU CHAI1 1Department of Respiratory, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121001; 2School of Public Health, Jilin University, Changchun, Jilin 130021; 3School of Pharmacy, Jiangxi University of Traditional Chinese Medicine, Nanchang, Jiangxi 330006, P.R.

Inositol pyrophosphates mediated the apoptosis induced by hypoxic injury in bone marrow-derived mesenchymal stem cells by autophagy.

Objective: To investigate the potential effect of IP7 on the autophagy and apoptosis of bone marrow mesenchymal stem cells (BM-MSCs) caused by hypoxia.

Methods: BM-MSCs isolated from adult male C57BL/6 mice were exposed to normoxic condition and hypoxic stress for 6 h, 12 h, and 24 h, respectively. Then, flow cytometry detected the characteristics of BM-MSCs.

CENPE promotes lung adenocarcinoma proliferation and is directly regulated by FOXM1.

Lung cancer is the most common and most lethal type of cancer. A sustained proliferative capacity is one of the hallmarks of cancer, and microtubules serve an important role in maintaining a sustained cell cycle. Therefore, understanding the regulation of microtubule proteins in the cell cycle is important for tumor prevention and treatment.