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Figure 7 | Critical Care

Figure 7

From: Endothelial dysfunction is a potential contributor to multiple organ failure and mortality in aged mice subjected to septic shock: preclinical studies in a murine model of cecal ligation and puncture

Figure 7

Potential pathways and mechanisms underlying the enhancement of endothelial dysfunction in aged mice subjected to sepsis. In aged blood vessels, septic shock induces an overwhelming degree of oxidative damage, leading to a marked degree of endothelial dysfunction, which, in turn, contributes to the MODS and mortality of sepsis. We hypothesize that part of the process involves the fact that in aged endothelial cell, oxidative stress is unable to induce an appropriate activation of the Nrf2/ARE pathway. Please see Discussion for additional details. ARE, antioxidant response element; BH4, tetrahydrobiopterin, a co-factor of eNOS; eNOS, endothelial isoform of NO synthase; iCa2+, intracellular calcium concentration; Keap1, Kelch-like erythroid cell-derived protein with CNC homology (ECH)-associated protein 1; MODS, multiple organ dysfunction syndrome; NO, nitric oxide; Nrf2, nuclear factor erythroid 2 (NF-E2)-related factor 2; PARP, poly(ADP-ribose) polymerase.

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Critical Care

ISSN: 1364-8535