Thelansis

 Ischemia-Reperfusion injury (IRI) is the exacerbated cellular dysfunction and death that occurs when blood flow is restored to previously ischemic tissues. While the re-establishment of blood flow is crucial for salvaging ischemic tissues, the reperfusion process paradoxically leads to further damage, posing a threat to the function and viability of the organ. IRI can affect various organs such as the heart, lungs, kidneys, gut, skeletal muscle, and brain. Additionally, it may impact the ischemic organ itself and induce systemic damage to distant organs, potentially resulting in multi-system organ failure. Reperfusion injury is a complex process involving multiple factors contributing to extensive tissue destruction. The pathophysiological mechanisms underlying ischemia-reperfusion injury have both local and systemic effects. This process occurs in two fundamental stages: during ischemia, the main factor at play is cellular energy depletion, and during reperfusion, there is an int...

 The myocardial ischemia-reperfusion syndrome is a complex entity where many inflammatory mediators play different roles in enhancing myocardial infarction-derived damage and healing the injury. In general terms, MIRS must be understood as a complex phenomenon that arises upon blood flow restoration, where reperfused leukocytes find many damage-associated molecular patterns (DAMPs), such as extracellular Ca+ and ATP released by necrotic cells, which induce the activation of many TLR pathways to promote an inflammatory response. Thus, an acute Th1 response is rapidly induced to clean the necrotic debris, but such an immune response, unfortunately, expands MI-associated damage. Myocardial reperfusion is unavoidable due to common MI treatments such as thrombolysis, angioplasty, and coronary bypass. Later, the Th1-immune response subsides to a Th2-driven immunity, where leukocytes shift their phenotype to orchestrate tissue remodeling to avoid cardiac rupture. Thelansis’s “Ischemia-R...