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Abstract: As an innate immune route of defense against microbial infringement, cyclic guanosine monophosphate (GMP)–adenosine monophosphate (AMP) synthase (cGAS)- stimulator of interferon genes (STING) signaling does not simply participate in amplifying inflammatory responses via releasing type-I interferon (IFN) or enhance the expression of pro-inflammatory genes, but also interplays with multifarious pathophysiological activities, such as autophagy, apoptosis, pyroptosis, ferroptosis, and senescence in a broad repertoire of cells like endothelial cells, macrophages and cardiomyocyte. Thus, the cGAS-STING pathway is closely linked with aberrant heart morphologically and functionally via these mechanisms. The past few decades have witnessed an increased interest in the exact relationship between the activation of the cGAS-STING pathway and the initiation or development of certain cardiovascular diseases (CVD). A group of scholars has gradually investigated the perturbation of myocardium affected by the overactivation or suppression of the cGAS-STING. This review focuses on how the cGAS-STING pathway interweaves with other pathways and creates a pattern of dysfunction associated with cardiac muscle. This sets treatments targeting the cGAS-STING pathway apart from traditional therapeutics for cardiomyopathy and achieves better clinical value.

Coronary artery spasm (CAS) plays an important role in the pathogenesis of ischemic heart disease. The clinical manifestations of CAS include variant angina, myocardial infarction and sudden death. Although endothelial dysfunction and hyperreactivity of vascular smooth muscle cells have been associated with CAS, the underlying mechanisms remain unclear. Thus, there is a long way to go to truly understand the pathogenesis of CAS to formulate effective treatments. This article discusses the pathophysiological mechanisms as well as downstream molecular pathways of CAS, with a focus on potential therapeutic targets.

Insomnia is a widespread sleep disorder in the general population, and it is a risk factor for impaired function, the development of other medical and mental disorders, and causes an increase in health care costs. In view of the health hazards of insomnia and the shortcomings of western medicine, Complementary and Alternative Medicine (CAM) should be considered in the management of insomnia. The present overview reports the potential role of herbal medicine and non-pharmacological therapies in the treatment of insomnia and summarizes the scientific evidence reported from 2008 to 2018. PubMed and Web of Science databases were searched for studies published from 2008 to 2018. 17 randomized controlled trials and 22 non-pharmacological therapies were included in this review, and the results showed that CAM had certain advantages in the treatment of insomnia. The safety of CAM for insomnia was acceptable. Meanwhile, based on pre-clinical trial, the possible mechanisms of CAM for insomnia were modulation of circadian rhythm, GABA receptor activation, antagonisms of 5-HT receptors, inhibition of glutamate-mediated pathways, and attenuation of inflammation. CAM for insomnia has made some progress, but high quality evidence-based medical evidence is still needed to provide guidance for clinical application.

Background Leaves of Ginkgo biloba, a "living fossil," have been used as traditional herbal medicine for hundreds of years in China. Currently, its application in vascular protection is garnering much attention. Methods In this manuscript, preclinical studies were reviewed to discuss various mechanisms underlying the vascular protection by Ginkgo biloba extract (GBE). Additionally, we reviewed clinical studies to present the application of GBE in the ischaemic disease. Results GBE, a commonly used dietary supplement, has been shown to act as an antioxidant and freeradical scavenger, a membrane stabilizer, an inhibitor of the platelet-activating factor, a vasodilator, and a regulator of metabolism. Currently, there exist a growing number of clinical studies about GBE in the application of cardiovascular disease, peripheral vascular disease (PVD) and diabetic vascular complications. Conclusion GBE, a promising therapeutic agent for cardiovascular and ischaemic diseases, exerts vascular- protection function by a comprehensive mechanisms.