Publications by authors named "Jin-Hua Bo"
Intervention of Asprosin Attenuates Oxidative Stress and Neointima Formation in Vascular Injury.
Antioxid Redox Signal
September 2024
Article Synopsis
- Asprosin is a recently identified hormone that contributes to insulin resistance and plays significant roles in promoting oxidative stress, proliferation, and migration in vascular smooth muscle cells (VSMCs) following vascular injury.* -
- In experiments using mouse aortic VSMCs and a model of carotid artery injury, asprosin overexpression was found to increase harmful effects like oxidative stress and VSMC proliferation, while the inhibition of its expression could reduce these negative outcomes and promote protective factors.* -
- Targeting asprosin could offer a potential therapeutic approach for treating vascular-related conditions, as its regulation is linked to the balance of various stress responses in injured arteries.*
Sympathetic overactivity contributes to the pathogenesis of sepsis. The selective α2-adrenergic receptor agonist dexmedetomidine (DEX) is widely used for perioperative sedation and analgesia. We aimed to determine the central roles and mechanisms of DEX in attenuating sympathetic activity and inflammation in sepsis.
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- The dorsal motor nucleus of the vagus (DMV) regulates vagal activity, but its role in sympathetic activity and the influence of salusin-β on autonomic function were previously unclear.
- In a study with male rats, salusin-β was found to inhibit renal sympathetic nerve activity (RSNA), enhance vagal activity, and lower blood pressure and heart rate through specific mechanisms linked to the production of superoxide anions in the intermediate DMV (iDMV).
- The effects of salusin-β included mediating sympathetic inhibition via both NAD(P)H oxidase-dependent actions and GABA receptor activation in the paraventricular nucleus (PVN), indicating its role in maintaining a balance between sympathetic and paras
Article Synopsis
- Extracellular vesicles (EVs) from vascular adventitial fibroblasts (AFs) promote the growth of vascular smooth muscle cells (VSMCs) and contribute to vascular changes in spontaneously hypertensive rats (SHR) through increased levels of the microRNA miR135a-5p.
- Inhibition of miR135a-5p prevents the proliferation of VSMCs by restoring the expression of its target gene, FNDC5, which is downregulated in SHR.
- The study indicates that targeting both miR135a-5p and FNDC5 could be potential strategies for treating VSMC proliferation related to hypertension.
Background: The mammalian target of rapamycin (mTOR) is known to regulate cell growth, and it also participates in pain transmission as has been recently verified in inflammatory and neuropathic pain models. The targeting of mTOR represents a new strategy for the control of chronic pain. In the present study, we investigated the effect of mTOR in the expression of PSD95 and NR2B-PSD95 or GluA2-PSD95 interaction ratio in a chronic constriction injury (CCI) mice model.
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