Cardiovascular Therapeutics and Ischemic Injury Mechanisms
Summary
Ischaemic injury underlies major cardiovascular events, encompassing myocardial infarction and stroke, and is characterised by reduced blood flow, oxygen deprivation and a cascade of cellular disturbances. Restoration of perfusion paradoxically exacerbates tissue damage through oxidative stress, calcium overload, mitochondrial dysfunction and sterile inflammation. Modern therapeutics aim to limit the infarct size, preserve microvascular integrity and prevent adverse remodelling. Strategies range from reperfusion techniques and anticoagulant or antiplatelet agents to novel molecular approaches that target key injury mediators such as reactive oxygen species, the mitochondrial permeability transition pore and inflammasome complexes. Adjunctive therapies including small-molecule inhibitors, biological agents and gene-based interventions seek to modulate apoptosis, autophagy and immune activation. Integrative approaches, incorporating traditional medicines and combination regimens, are under evaluation for synergistic benefits. Advances in drug delivery systems, biomarker-guided treatment and personalised cardiovascular care are driving progress towards minimising long-term morbidity and mortality associated with ischaemic events.
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Cardiovascular Therapeutics and Ischemic Injury Mechanisms publication trend
The graph below shows the total number of articles in cardiovascular therapeutics and ischemic injury mechanisms across all publications each year (not limited to Nature Index journals).
Technical terms
Ischaemia/reperfusion injury: Tissue damage occurring when blood supply returns to ischaemic tissue, triggering oxidative stress and inflammation.
Inflammasome: A multiprotein intracellular complex that activates inflammatory cytokines in response to cellular stress.
Reactive oxygen species (ROS): Chemically reactive molecules derived from oxygen that can damage proteins, lipids and DNA.
Mitochondrial permeability transition pore (mPTP): A non-specific channel whose opening disrupts mitochondrial membrane potential and initiates cell death.
Left ventricular ejection fraction: The percentage of blood expelled from the left ventricle with each heartbeat, used as a measure of cardiac pump function.
References
- Comprehensive effect of Naoxintong capsule combined with Western medicine on coronary heart disease after percutaneous coronary intervention: a meta-analysis. Frontiers in Pharmacology (2024).
- Characterization of the Components and Metabolites of Achyranthes Bidentata in the Plasma and Brain Tissue of Rats Based on Ultrahigh Performance Liquid Chromatography–High-Resolution Mass Spectrometry (UHPLC–HR-MS). Molecules (2024).
- Naoxintong attenuates Ischaemia/reperfusion Injury through inhibiting NLRP3 inflammasome activation. Journal of Cellular and Molecular Medicine (2016).
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