Heparan Sulfate Induces Necroptosis in Murine Cardiomyocytes: A Medical-in-Silico Approach Combining In Vitro Experiments and Machine Learning (vol 9, 393, 2018)

A Corrigendum on Heparan Sulfate Induces Necroptosis in Murine Cardiomyocytes: A Medical-In silico Approach Combining In vitro Experiments and Machine Learning by Zechendorf E, Vaßen P, Zhang J, Hallawa A, Martincuks A, Krenkel O, Müller-Newen G, Schuerholz T, Simon T-P, Marx G, Ascheid G, Schmeink A, Dartmann G, Thiemermann C and Martin L (2018). Front. Immunol. 9:393. doi: 10.3389/fimmu.2018.00393 In the original article, there was an error in the Author Contributions section. The wording used to declare the contribution of Elisabeth Zechendorf was not clear. The new Author Contributions section appears below. Conception and design: EZ, LM, GD, AS, and CT. In vitro experiments and data analyses: EZ, LM, TS, T-PS, AM, GM-N, OK, GM, and PV. Medical in silico experiments and data analyses: EZ, PV, JZ, GD, AS, LM, AH, and GA. EZ wrote the manuscript. Correction of the manuscript: EZ, PV, LM, CT, GM, GD, T-PS, and AS. All the authors reviewed and finally approved the manuscript. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated

Ribonuclease 1 attenuates septic cardiomyopathy and cardiac apoptosis in a murine model of polymicrobial sepsis.

Septic cardiomyopathy is a life-threatening organ dysfunction caused by sepsis. Ribonuclease 1 (RNase 1) belongs to a group of host-defense peptides that specifically cleave extracellular RNA (eRNA). The activity of RNase1 is inhibited by ribonuclease-inhibitor 1 (RNH1). The role of RNase 1 in septic cardiomyopathy and associated cardiac apoptosis, however, is completely unknown. Here, we showed that sepsis resulted in a significant increase in RNH1 and eRNA serum levels compared to those of healthy subjects (p < 0.05). Treatment with RNase 1 resulted in a significant decrease of apoptosis, induced by the intrinsic pathway, and TNF expression in murine cardiomyocytes exposed to either necrotic cardiomyocytes or serum of septic patients for 16 h (p < 0.05). Furthermore, treatment of septic mice with RNase 1 resulted in a reduction in cardiac apoptosis, TNF expression and septic cardiomyopathy (p < 0.05). These data demonstrate that eRNA plays a crucial role in the pathophysiology of the organ (cardiac) dysfunction in sepsis and RNase and RNH1 may be new therapeutic targets/strategies to reduce the cardiac injury and dysfunction caused by sepsis