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Protective effects of berbamine against arginase-1 deficiency-induced injury in human brain microvascular endothelial cells.

Front Pharmacol

January 2025

Department of Geriatric Medicine, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, Guangdong, China.

Endothelial cell dysfunction plays a crucial role in the early development of cerebral small vessel disease (CSVD). Arginase-1 (ARG1) is expressed in endothelial cells, and its deficiency may exacerbate cerebrovascular damage by increasing reactive oxygen species (ROS) production, thereby inducing endothelial cell apoptosis. Berbamine (BBM) has shown potential in neuroprotection and cardiovascular disease prevention.

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Mesenchymal stem cells derived exosomes: a new era in cardiac regeneration.

Stem Cell Res Ther

January 2025

Department of Tissue Engineering and Applied Cell Sciences, School of Advanced Medical Sciences and Technologies, Shiraz University of Medical Sciences, Shiraz, Iran.

Despite significant strides in medical treatments and surgical procedures for cardiovascular diseases, these conditions continue to be a major global health concern. The persistent need for innovative therapeutic approaches to mend damaged heart tissue highlights the complexity and urgency of this medical challenge. In recent years, stem cells have emerged as a promising tool for tissue regeneration, but challenges such as graft rejection and tumor formation have limited their clinical application.

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Long non-coding RNAs (lncRNAs) are among the most abundant types of non-coding RNAs in the genome and exhibit particularly high expression levels in the brain, where they play crucial roles in various neurophysiological and neuropathological processes. Although ischemic stroke is a complex multifactorial disease, the involvement of brain-derived lncRNAs in its intricate regulatory networks remains inadequately understood. In this study, we established a cerebral ischemia-reperfusion injury model using middle cerebral artery occlusion (MCAO) in male Sprague-Dawley rats.

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Vascular diseases, such as hypertension, atherosclerosis, cerebrovascular, and peripheral arterial diseases, present major clinical and public health challenges, largely due to their common underlying process: vascular remodeling. This process involves structural alterations in blood vessels, driven by a variety of molecular mechanisms. The inhibitor of DNA-binding/differentiation-3 (), a crucial member of ID family of transcriptional regulators, has been identified as a key player in vascular biology, significantly impacting the progression of these diseases.

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Diabetes mellitus can cause impaired and delayed wound healing, leading to lower extremity amputations; however, the mechanisms underlying the regulation of vascular endothelial growth factor-dependent (VEGF-dependent) angiogenesis remain unclear. In our study, the molecular underpinnings of endothelial dysfunction in diabetes are investigated, focusing on the roles of disabled-2 (Dab2) and Forkhead box M1 (FOXM1) in VEGF receptor 2 (VEGFR2) signaling and endothelial cell function. Bulk RNA-sequencing analysis identified significant downregulation of Dab2 in high-glucose-treated primary mouse skin endothelial cells.

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