Figure 1

1.Singer, M. et al. The third worldwide consensus definitions for sepsis and septic shock (Sepsis-Three). JAMA 315, 801–810, https://doi.org/10.1001/jama.2016.0287 (2016).2.Shankar-Hari, M. et al. Creating a brand new definition and assessing new medical standards for septic shock: for the Third Worldwide Consensus Definitions for Sepsis and Septic Shock (Sepsis-Three). JAMA 315, 775–787, https://doi.org/10.1001/jama.2016.0289 (2016).Three.Seymour, C. W. et al. Evaluation of medical standards for cepsis: for the Third Worldwide Consensus Definitions for Sepsis and Septic Shock (Sepsis-Three). JAMA 315, 762–774, https://doi.org/10.1001/jama.2016.0288 (2016).Four.Fleischmann, C. et al. Evaluation of world incidence and mortality of hospital-treated sepsis. Present estimates and limitations. Am J Respir Crit Care Med 193, 259–272, https://doi.org/10.1164/rccm.201504-0781OC (2016).5.Corridor, M. J., Williams, S. N., DeFrances, C. J. & Golosinskiy, A. 1–eight (Nationwide Middle for Well being Statistics Hyattsville, MD, 2011).6.Levy, M. M. et al. The Surviving Sepsis Marketing campaign: outcomes of a world guideline-based efficiency enchancment program focusing on extreme sepsis. Crit Care Med 38, 367–374, https://doi.org/10.1097/CCM.0b013e3181cb0cdc (2010).7.Masewu, A. et al. Acute kidney harm is a strong unbiased predictor of mortality in critically in poor health sufferers: a multicenter potential cohort examine from Kinshasa, the Democratic Republic of Congo. BMC Nephrol 17, 118, https://doi.org/10.1186/s12882-016-0333-Four (2016).eight.Sevransky, J. E. et al. Pulmonary vs nonpulmonary sepsis and mortality in acute lung harm. Chest 134, 534–538, https://doi.org/10.1378/chest.08-Zero309 (2008).9.Martin, G. S., Mannino, D. M. & Moss, M. The impact of age on the event and end result of grownup sepsis. Crit Care Med 34, 15–21, doi:00003246-200601000-Zero0003 [pii] (2006).10.Dombrovskiy, V. Y., Martin, A. A., Sunderram, J. & Paz, H. L. Fast enhance in hospitalization and mortality charges for extreme sepsis in america: a pattern evaluation from 1993 to 2003. Crit Care Med 35, 1244–1250, https://doi.org/10.1097/01.CCM.0000261890.41311.E9 (2007).11.US Meals and Drug Administration. (Silver Spring, MD, 2011).12.Gotts, J. E. & Matthay, M. A. Sepsis: pathophysiology and medical administration. BMJ 353, i1585, https://doi.org/10.1136/bmj.i1585 (2016).13.Khan, M. M., Yang, W. L., Brenner, M., Bolognese, A. C. & Wang, P. Chilly-inducible RNA-binding protein (CIRP) causes sepsis-associated acute lung harm through induction of endoplasmic reticulum stress. Sci Rep 7, 41363, https://doi.org/10.1038/srep41363 (2017).14.Wellmann, S. et al. Oxygen-regulated expression of the RNA-binding proteins RBM3 and CIRP by a HIF-1-independent mechanism. J Cell Sci 117, 1785–1794, https://doi.org/10.1242/jcs.01026 (2004).15.Al-Fageeh, M. B. & Smales, C. M. Various promoters regulate chilly inducible RNA-binding (CIRP) gene expression and improve transgene expression in mammalian cells. Mol Biotechnol 54, 238–249, https://doi.org/10.1007/s12033-013-9649-5 (2013).16.De Leeuw, F. et al. The cold-inducible RNA-binding protein migrates from the nucleus to cytoplasmic stress granules by a methylation-dependent mechanism and acts as a translational repressor. Exp Cell Res 313, 4130–4144, https://doi.org/10.1016/j.yexcr.2007.09.Zero17 (2007).17.Morf, J. et al. Chilly-inducible RNA-binding protein modulates circadian gene expression posttranscriptionally. Science 338, 379–383, https://doi.org/10.1126/science.1217726 (2012).18.Qiang, X. et al. Chilly-inducible RNA-binding protein (CIRP) triggers inflammatory responses in hemorrhagic shock and sepsis. Nat Med 19, 1489–1495, https://doi.org/10.1038/nm.3368 (2013).19.Zhou, Y. et al. The cold-inducible RNA-binding protein (CIRP) stage in peripheral blood predicts sepsis end result. PLoS One 10, e0137721, https://doi.org/10.1371/journal.pone.0137721 (2015).20.Yang, W. L. et al. Chilly-inducible RNA-binding protein causes endothelial dysfunction through activation of Nlrp3 inflammasome. Sci Rep 6, 26571, https://doi.org/10.1038/srep26571 (2016).21.Aird, W. C. The function of the endothelium in extreme sepsis and a number of organ dysfunction syndrome. Blood 101, 3765–3777, https://doi.org/10.1182/blood-2002-06-1887 (2003).22.Cen, C. et al. Deficiency of cold-inducible ribonucleic acid-binding protein reduces renal harm after ischemia-reperfusion. Surgical procedure 160, 473–483, https://doi.org/10.1016/j.surg.2016.04.Zero14 (2016).23.Shin, H. J. et al. Kinetics of binding of LPS to recombinant CD14, TLR4, and MD-2 proteins. Mol Cells 24, 119–124 (2007).24.Yang, H. et al. A vital cysteine is required for HMGB1 binding to Toll-like receptor Four and activation of macrophage cytokine launch. Proc Natl Acad Sci USA 107, 11942–11947, https://doi.org/10.1073/pnas.1003893107 (2010).25.Angele, M. Ok., Schwacha, M. G., Ayala, A. & Chaudry, I. H. Impact of gender and intercourse hormones on immune responses following shock. Shock 14, 81–90 (2000).26.Diodato, M. D., Knoferl, M. W., Schwacha, M. G., Bland, Ok. I. & Chaudry, I. H. Gender variations within the inflammatory response and survival following haemorrhage and subsequent sepsis. Cytokine 14, 162–169, https://doi.org/10.1006/cyto.2001.0861 (2001).27.Luiking, Y. C., Hallemeesch, M. M., Vissers, Y. L., Lamers, W. H. & Deutz, N. E. In vivo entire physique and organ arginine metabolism throughout endotoxemia (sepsis) depends on mouse pressure and gender. J Nutr 134, 2768S–2774S, dialogue 2796S–2797S (2004).28.Aoyama, M., Kotani, J. & Usami, M. Gender distinction in granulocyte dynamics and apoptosis and the function of IL-18 throughout endotoxin-induced systemic irritation. Shock 32, 401–409, https://doi.org/10.1097/SHK.0b013e31819c358a (2009).29.Zhang, F., Yang, W.-L., Brenner, M. & Wang, P. Attenuation of hemorrhage-associated lung harm by adjuvant therapy with C23, an oligopeptide derived from cold-inducible RNA-binding protein (CIRP). J Trauma Acute Care Surg. https://doi.org/10.1097/TA.0000000000001566 (2017).30.Hirano, Y. et al. Neutralization of osteopontin attenuates neutrophil migration in sepsis-induced acute lung harm. Crit Care 19, 53, https://doi.org/10.1186/s13054-Zero15-0782-Three (2015).31.Livak, Ok. J. & Schmittgen, T. D. Evaluation of relative gene expression knowledge utilizing real-time quantitative PCR and the two(-Delta Delta C(T)) Technique. Strategies 25, 402–408, https://doi.org/10.1006/meth.2001.1262 (2001).32.Giannini, E. G., Testa, R. & Savarino, V. Liver enzyme alteration: a information for clinicians. CMAJ 172, 367–379, https://doi.org/10.1503/cmaj.1040752 (2005).33.Nishiyama, H. et al. Cloning and characterization of human CIRP (cold-inducible RNA-binding protein) cDNA and chromosomal task of the gene. Gene 204, 115–120, doi:S0378-1119(97)00530-1 [pii] (1997).34.Yang, C. & Service, F. The UV-inducible RNA-binding protein A18 (A18 hnRNP) performs a protecting function within the genotoxic stress response. J Biol Chem 276, 47277–47284, https://doi.org/10.1074/jbc.M105396200 (2001).35.Yang, R. et al. Useful significance for a heterogenous ribonucleoprotein A18 signature RNA motif within the Three′-untranslated area of ataxia telangiectasia mutated and Rad3-related (ATR) transcript. J Biol Chem 285, 8887–8893, https://doi.org/10.1074/jbc.M109.013128 (2010).36.Nishiyama, H. et al. Decreased expression of cold-inducible RNA-binding protein (CIRP) in male germ cells at elevated temperature. Am J Pathol 152, 289–296 (1998).37.Nishiyama, H. et al. Diurnal change of the cold-inducible RNA-binding protein (Cirp) expression in mouse mind. Biochem Biophys Res Commun 245, 534–538, https://doi.org/10.1006/bbrc.1998.8482 (1998).38.Xue, J. H. et al. Results of ischemia and H2O2 on the chilly stress protein CIRP expression in rat neuronal cells. Free Radic Biol Med 27, 1238-1244, doi:S0891-5849(99)00158-6 [pii] (1999).39.Fornace, A. J. Jr, Alamo, I. Jr. & Hollander, M. C. DNA damage-inducible transcripts in mammalian cells. Proc Natl Acad Sci USA 85, 8800–8804 (1988).40.Sheikh, M. S. et al. Identification of a number of human homologs of hamster DNA damage-inducible transcripts. Cloning and characterization of a novel UV-inducible cDNA that codes for a putative RNA-binding protein. J Biol Chem 272, 26720–26726 (1997).41.Barenco, M. et al. Ranked prediction of p53 targets utilizing hidden variable dynamic modeling. Genome biology 7, R25, https://doi.org/10.1186/gb-2006-7-Three-r25 (2006).42.Godwin, A. et al. Blocking cold-inducible RNA-binding protein protects liver from ischemia-reperfusion harm. Shock 43, 24–30, https://doi.org/10.1097/SHK.0000000000000251 (2015).43.Zhou, M., Yang, W. L., Ji, Y., Qiang, X. & Wang, P. Chilly-inducible RNA-binding protein mediates neuroinflammation in cerebral ischemia. Biochim Biophys Acta 1840, 2253–2261. https://doi.org/10.1016/j.bbagen.2014.02.027 (2014).44.Nesseler, N. et al. Scientific assessment: The liver in sepsis. Crit Care 16, 235, https://doi.org/10.1186/cc11381 (2012).45.Kellum, J. A. et al. Understanding the inflammatory cytokine response in pneumonia and sepsis: outcomes of the Genetic and Inflammatory Markers of Sepsis (GenIMS) Examine. Arch Intern Med 167, 1655–1663, https://doi.org/10.1001/archinte.167.15.1655 (2007).46.Hwaiz, R. et al. Rac1 signaling regulates sepsis-induced pathologic irritation within the lung through attenuation of Mac-1 expression and CXC chemokine formation. J Surg Res 183, 798–807, https://doi.org/10.1016/j.jss.2013.02.045 (2013).47.Dolinay, T. et al. Inflammasome-regulated cytokines are vital mediators of acute lung harm. Am J Respir Crit Care Med 185, 1225–1234, https://doi.org/10.1164/rccm.201201-0003OC (2012).48.Rudkowski, J. C. et al. Roles of iNOS and nNOS in sepsis-induced pulmonary apoptosis. Am J Physiol Lung Cell Mol Physiol 286, L793–800, https://doi.org/10.1152/ajplung.Zero0266.2003 (2004).49.Gill, S. E., Rohan, M. & Mehta, S. Function of pulmonary microvascular endothelial cell apoptosis in murine sepsis-induced lung harm in vivo. Respir Res 16, 109, https://doi.org/10.1186/s12931-Zero15-0266-7 (2015).50.Zhang, H. T. et al. Chilly-inducible RNA-binding protein inhibits neuron apoptosis by the suppression of mitochondrial apoptosis. Mind Res 1622, 474–483, https://doi.org/10.1016/j.brainres.2015.07.Zero04 (2015).51.Lujan, D. A. et al. Chilly-inducible RNA binding protein in mouse mammary gland growth. Tissue & cell 48, 577–588. https://doi.org/10.1016/j.tice.2016.10.Zero04 (2016).52.Lee, H. N., Ahn, S. M. & Jang, H. H. Chilly-inducible RNA-binding protein, CIRP, inhibits DNA damage-induced apoptosis by regulating p53. Biochem Biophys Res Commun 464, 916–921, https://doi.org/10.1016/j.bbrc.2015.07.Zero66 (2015).53.Liao, Y., Feng, J., Zhang, Y., Tang, L. & Wu, S. The mechanism of CIRP in inhibition of keratinocytes development arrest and apoptosis following low dose UVB radiation. Mol Carcinog 56, 1554–1569, https://doi.org/10.1002/mc.22597 (2017).54.Han, W. Ok. et al. Urinary biomarkers within the early prognosis of acute kidney harm. Kidney Int 73, 863–869, https://doi.org/10.1038/sj.ki.5002715 (2008).55.Han, M., Li, Y., Liu, M., Li, Y. & Cong, B. Renal neutrophil gelatinase related lipocalin expression in lipopolysaccharide-induced acute kidney harm within the rat. BMC Nephrol 13, 25, https://doi.org/10.1186/1471-2369-13-25 (2012).56.Ko, G. J. et al. Transcriptional evaluation of kidneys throughout restore from AKI reveals attainable roles for NGAL and KIM-1 as biomarkers of AKI-to-CKD transition. Am J Physiol Renal Physiol 298, F1472–1483, https://doi.org/10.1152/ajprenal.00619.2009 (2010).57.Sprenkle, P. & Russo, P. Molecular markers for ischemia, do we now have one thing higher then creatinine and glomerular filtration charge? Arch Esp Urol 66, 99–114 (2013).58.Zhang, M. et al. Toll-like receptor Four is important to preserving cardiac perform and survival in low-grade polymicrobial sepsis. Anesthesiology 121, 1270–1280, https://doi.org/10.1097/ALN.0000000000000337 (2014).59.Deng, M. et al. Lipopolysaccharide clearance, bacterial clearance, and systemic inflammatory responses are regulated by cell type-specific capabilities of TLR4 throughout sepsis. J Immunol 190, 5152–5160, https://doi.org/10.4049/jimmunol.1300496 (2013).60.Entezari, M. et al. Inhibition of high-mobility group field 1 protein (HMGB1) enhances bacterial clearance and protects in opposition to Pseudomonas Aeruginosa pneumonia in cystic fibrosis. Mol Med 18, 477–485, https://doi.org/10.2119/molmed.2012.00024 (2012).61.Rice, T. W. et al. A randomized, double-blind, placebo-controlled trial of TAK-242 for the therapy of extreme sepsis. Crit Care Med 38, 1685–1694, https://doi.org/10.1097/CCM.0b013e3181e7c5c9 (2010).62.Opal, S. M. et al. Impact of eritoran, an antagonist of MD2-TLR4, on mortality in sufferers with extreme sepsis: the ACCESS randomized trial. JAMA 309, 1154–1162, https://doi.org/10.1001/jama.2013.2194 (2013).63.Sakurai, T. et al. Cirp protects in opposition to tumor necrosis factor-alpha-induced apoptosis through activation of extracellular signal-regulated kinase. Biochim Biophys Acta 1763, 290–295, https://doi.org/10.1016/j.bbamcr.2006.02.007 (2006).64.Masuda, T. et al. Chilly-inducible RNA-binding protein (Cirp) interacts with Dyrk1b/Mirk and promotes proliferation of immature male germ cells in mice. Proc Natl Acad Sci USA 109, 10885–10890, https://doi.org/10.1073/pnas.1121524109 (2012).

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