Gaseous signalling molecules, including nitric oxide (NO), molecular hydrogen (H2), hydrogen sulfide (H2S), and carbon monoxide (CO), and gas donor molecules thereof, have been emerging as potentially promising cardiovascular pharmacological candidates over the past years due to increasing experimental findings regarding their evident benefits to the cardiovascular system, as well as their peculiar advantages, such as smaller molecular weight, relatively higher safety, and widespread sources in nature. The cardiovascular therapeutic potential has been in a range of conditions, such as myocardial ischemic injury, atherosclerosis, and hypertension. Further in-depth research on the cardiovascular effect and mechanisms of these gaseous signalling molecules would facilitate the understanding of their biological significance theoretically, and thereby inform their translational application clinically.
Despite the self-evident biomedical effects of the gaseous signalling molecules with respect to cardiovascular conditions, the precise molecular mechanisms underlying the biological effects, however, are largely elusive, which greatly slows down the progression of relevant clinical trials and further limits their clinical translation and application. In this research topic, we aim to collect studies that propose a novel and detailed mechanism to support a well-documented or not yet reported cardiovascular effect. Studies involving physically molecule-molecule direct interactions, or confirming novel and specific targets, or identifying and further corroborating a distinctive genetic, epigenetic, and signalling process on the basis of high-throughput screening are most welcome.
In this article collection, we invite submissions in the form of Original Research, Reviews, and Mini-Reviews, that clarify the pharmacological effect and novel molecular or cellular mechanism of gaseous signalling molecules. We encourage submissions dealing with one or more of, but not limited to the following themes:
• Effect and molecular mechanism of gaseous signalling molecules in cardiovascular diseases;
• Endogenous gaseous signalling molecules as potentially important mechanisms mediating pharmacological effects of cardiovascular agents;
• Genetic, epigenetic, and signalling pathways related to the implication of gaseous signalling molecules in cardiovascular diseases;
• Novel and specific targets by which gaseous signalling molecules exert their cardiovascular effect.
• Omics and system biology strategies in a combination of experimental validation to identify the most salient mechanism underlying the effects of gaseous signalling molecules within the cardiovascular system.
Gaseous signalling molecules, including nitric oxide (NO), molecular hydrogen (H2), hydrogen sulfide (H2S), and carbon monoxide (CO), and gas donor molecules thereof, have been emerging as potentially promising cardiovascular pharmacological candidates over the past years due to increasing experimental findings regarding their evident benefits to the cardiovascular system, as well as their peculiar advantages, such as smaller molecular weight, relatively higher safety, and widespread sources in nature. The cardiovascular therapeutic potential has been in a range of conditions, such as myocardial ischemic injury, atherosclerosis, and hypertension. Further in-depth research on the cardiovascular effect and mechanisms of these gaseous signalling molecules would facilitate the understanding of their biological significance theoretically, and thereby inform their translational application clinically.
Despite the self-evident biomedical effects of the gaseous signalling molecules with respect to cardiovascular conditions, the precise molecular mechanisms underlying the biological effects, however, are largely elusive, which greatly slows down the progression of relevant clinical trials and further limits their clinical translation and application. In this research topic, we aim to collect studies that propose a novel and detailed mechanism to support a well-documented or not yet reported cardiovascular effect. Studies involving physically molecule-molecule direct interactions, or confirming novel and specific targets, or identifying and further corroborating a distinctive genetic, epigenetic, and signalling process on the basis of high-throughput screening are most welcome.
In this article collection, we invite submissions in the form of Original Research, Reviews, and Mini-Reviews, that clarify the pharmacological effect and novel molecular or cellular mechanism of gaseous signalling molecules. We encourage submissions dealing with one or more of, but not limited to the following themes:
• Effect and molecular mechanism of gaseous signalling molecules in cardiovascular diseases;
• Endogenous gaseous signalling molecules as potentially important mechanisms mediating pharmacological effects of cardiovascular agents;
• Genetic, epigenetic, and signalling pathways related to the implication of gaseous signalling molecules in cardiovascular diseases;
• Novel and specific targets by which gaseous signalling molecules exert their cardiovascular effect.
• Omics and system biology strategies in a combination of experimental validation to identify the most salient mechanism underlying the effects of gaseous signalling molecules within the cardiovascular system.
