As the leading causes of death worldwide, cardiovascular diseases (CVDs) include hypertension, atherosclerosis, aneurysm, cardiomyopathy, coronary artery heart diseases, heart failure, etc. Remodeling in the heart and arteries is the basic pathological changes in CVDs, and it also contributes to the progress and deterioration of CVDs. Smoking, unhealthy diet, physical inactivity, metabolic syndrome, and high blood pressure are the most common risk factors for CVDs. The pathogenesis of CVDs is diverse and complex, with inflammation and oxidative stress playing the most crucial roles. For instance, in ischemic cardiac diseases, inflammation and oxidative stress play crucial roles in mediating cell death as well as recruiting immune cells to the necrotic area, engulfing cell debris, and initiating the repair process to avoid cardiac rupture. Inflammation and oxidative stress are also vital hallmarks during atherogenesis and vascular aging which have been successfully developed as therapeutic targets for the treatment of these diseases.
Many attempts have been made to identify new therapeutic targets and new drugs for CVDs, especially after the wide application of single-cell sequencing, macromolecular docking, high-throughput drug screening, and artificial intelligence technology. In this research topic, we intended to focus on the pathophysiological mechanism, and clinical significance of inflammation, oxidative stress, and cell death (necrosis and programmed cell death, such as pyroptosis, ferroptosis and PANoptosis) in CVDs. We welcome researches about the pharmacological interventions, lifestyle modifications, and novel treatment modalities that aim to restore cardiovascular health by modulating these interconnected pathways. Translational studies, clinical trials, and insights from experts in the field are all welcomed.
Areas of interest include but are not limited to the following aspects:
1. Novel mechanistic insights on how inflammation, oxidative stress, remodeling and cell death develop in CVDs.
2. The crosstalk between inflammation, oxidative stress and cell death (necrosis and programmed cell death) in CVDs.
3. Novel strategies for the evaluation of inflammation, oxidative stress, remodeling and cell death in CVD patients and their clinical significance.
4. Drug discoveries or novel treatment approaches (drugs, nanomaterials, and others) in CVDs through targeting inflammation and oxidative stress.
5. Drug discoveries or novel treatment approaches (drugs, nanomaterials, and others) in CVDs through targeting remodeling and cell death.
As the leading causes of death worldwide, cardiovascular diseases (CVDs) include hypertension, atherosclerosis, aneurysm, cardiomyopathy, coronary artery heart diseases, heart failure, etc. Remodeling in the heart and arteries is the basic pathological changes in CVDs, and it also contributes to the progress and deterioration of CVDs. Smoking, unhealthy diet, physical inactivity, metabolic syndrome, and high blood pressure are the most common risk factors for CVDs. The pathogenesis of CVDs is diverse and complex, with inflammation and oxidative stress playing the most crucial roles. For instance, in ischemic cardiac diseases, inflammation and oxidative stress play crucial roles in mediating cell death as well as recruiting immune cells to the necrotic area, engulfing cell debris, and initiating the repair process to avoid cardiac rupture. Inflammation and oxidative stress are also vital hallmarks during atherogenesis and vascular aging which have been successfully developed as therapeutic targets for the treatment of these diseases.
Many attempts have been made to identify new therapeutic targets and new drugs for CVDs, especially after the wide application of single-cell sequencing, macromolecular docking, high-throughput drug screening, and artificial intelligence technology. In this research topic, we intended to focus on the pathophysiological mechanism, and clinical significance of inflammation, oxidative stress, and cell death (necrosis and programmed cell death, such as pyroptosis, ferroptosis and PANoptosis) in CVDs. We welcome researches about the pharmacological interventions, lifestyle modifications, and novel treatment modalities that aim to restore cardiovascular health by modulating these interconnected pathways. Translational studies, clinical trials, and insights from experts in the field are all welcomed.
Areas of interest include but are not limited to the following aspects:
1. Novel mechanistic insights on how inflammation, oxidative stress, remodeling and cell death develop in CVDs.
2. The crosstalk between inflammation, oxidative stress and cell death (necrosis and programmed cell death) in CVDs.
3. Novel strategies for the evaluation of inflammation, oxidative stress, remodeling and cell death in CVD patients and their clinical significance.
4. Drug discoveries or novel treatment approaches (drugs, nanomaterials, and others) in CVDs through targeting inflammation and oxidative stress.
5. Drug discoveries or novel treatment approaches (drugs, nanomaterials, and others) in CVDs through targeting remodeling and cell death.
