BACKGROUND Mitochondria-mediated cell death plays a critical role in myocardial ischemia-reperfusion (IR) injury. We hypothesized that nanoparticle-mediated drug delivery of mitochondrial division inhibitor 1 (Mdivi1) protects hearts from IR injury through inhibition of mitochondria outer membrane permeabilization (MOMP), which causes mitochondrial-mediated cell death. METHODS AND RESULTS We ...

Objectives The objectives of the current study were to evaluate the effects of hepatic ischemia/reperfusion (IR) injury on the activity of antioxidant enzymes, biochemical factors, and histopathological changes in rat kidney, and to investigate the effect of crocin on IR-related changes. Materials and Methods Thirty-two male Wistar rats were randomly allocated into four groups (n=8). They wer...

3. Li Volti G, Sorrenti V, Murabito P et al. Pharmacological induction of heme oxygenase-1 inhibits iNOS and oxidative stress in renal ischemiareperfusion injury. Transplant Proc 2007; 39: 2986–2991 4. Datta PK, Koukouritaki SB, Hopp KA et al. Heme oxygenase-1 induction attenuates inducible nitric oxide synthase expression and proteinuria in glomerulonephritis. J Am Soc Nephrol 1999; 10: 2540–2...

We read with interest the study by Christiansen and colleagues [1] in the previous issue of Critical Care. In a large cohort study, the authors report that among diabetic patients who are admitted to the ICU, the preadmission use of metformin is associated with a lower mortality rate. Here, we highlight that metformin limits ischemiareperfusion injury (IRI) and modulates inflammation by increas...

Peroxisome proliferator-activated receptors (PPARs) are members of the nuclear hormone receptor superfamily that regulate the expression of genes involved in a variety of biological processes, including lipid metabolism and insulin sensitivity. Members of the PPAR family—in particular, PPAR—have more recently been shown to broadly regulate inflammatory and reparative responses. PPARis expressed...

Calpain 1 (CPN1) is a ubiquitous cysteine protease that exists in both cytosol and cardiac mitochondria. Mitochondrial CPN1 (mit-CPN1) is located in the intermembrane space and matrix. Activation of mit-CPN1 within the intermembrane space increases cardiac injury by releasing apoptosis-inducing factor from mitochondria during ischemia-reperfusion (IR). We asked if activation of mit-CPN1 is invo...

Intestinal ischemia-reperfusion (IR) injury is initiated when natural Abs recognize neoantigens that are revealed on ischemic cells. Cr2(-/-) mice, deficient in complement receptors (CR)1 and CR2, demonstrate defects in T-dependent B-2 B cell responses to foreign Ags and have also been suggested to manifest abnormalities of the B-1 subset of B lymphocytes. To determine whether these CRs might p...

BACKGROUND Novel treatment strategies are required to reduce the development of hepatic injury during surgical procedure in which renal ischemia/reperfusion (IR) is inevitable. Remote perconditioning (rPeC) has been proved to reduce the extent of kidney damages induced by renal IR injury. The aim of this study was to determine the protective effect of rPeC against hepatic injury caused by renal...

After complement system (CS) activation, the sequential production of complement products increases cell injury and death through opsonophagocytosis, cytolysis, adaptive, and inflammatory cell responses. These responses potentiate cerebral ischemia-reperfusion (IR) injury after ischemic stroke and reperfusion. Activation of the CS via mannose binding lectin (MBL)-initiated lectin pathway is kno...

Fibroblast growth factor 2 (FGF2) is cardioprotective in in vivo models of myocardial infarction; however, whether FGF2 has a protective role in in vivo ischemia-reperfusion (IR) injury, a model that more closely mimics acute myocardial infarction in humans, is not known. To assess the cardioprotective efficacy of endogenous FGF2, mice lacking a functional Fgf2 gene (Fgf2(-/-)) and wild-type co...