Inflammatory response in reperfusion injury

Inflammatory response in reperfusion injury describes the complex cascade of immune and inflammatory changes triggered when blood supply returns to tissue after a period of ischemia (lack of oxygen), such as after myocardial infarction, stroke, or organ transplantation[1][2][3][4][5][6][7]. Upon reperfusion, tissue-resident macrophages, endothelial cells, and recruited circulating leukocytes (especially neutrophils and monocytes) are activated by damage-associated molecular patterns (DAMPs) released from injured cells[2][3][7]. These DAMPs bind to pattern recognition receptors such as Toll-like receptors (TLRs), initiating signaling pathways that drive the production of pro-inflammatory cytokines (e.g., IL-6, TNF-α), chemokines, and reactive oxygen species (ROS)[2][3][4][7]. The resulting local and systemic inflammation increases vascular permeability, attracts additional immune cells, and amplifies tissue injury through direct cytotoxicity and apoptosis, often worsening the initial ischemic damage. This response is central to the pathogenesis of conditions like myocardial ischemia/reperfusion injury (MIRI), acute kidney injury, and post-transplant organ dysfunction[1][2][3][4][5][6][7].

Other names

Ischemia-reperfusion inflammatory responseSterile inflammation in reperfusion injury