[Corrigendum] Effects of simvastatin on iNOS and caspase‑3 levels and oxidative stress following smoke inhalation injury.

After the publication of the above paper, the authors have noticed that the affiliations were presented incorrectly; essentially, Drs Rong‑qiang Yang, Peng‑fei Guo, Qing‑nan Meng, Ya Gao, Imran Khan, Xiao‑bo Wang and Zheng‑jun Cui are based at the Department of Burn and Repair Reconstruction Surgery, The First Affiliated Hospital of Zhengzhou University, whereas Drs Zhao Ma and Cheng Chang are located at The School of Basic Medical Science of Zhengzhou University. Therefore, the affiliations for this paper should have appeared as follows: Rong‑Qiang Yang1, Peng‑Fei Guo1, Zhao Ma2, Cheng Chang2, Qing‑Nan Meng1, Ya Gao1, Imran Khan1, Xiao‑Bo Wang1 and Zheng‑Jun Cui1. 1Department of Burn and Repair Reconstruction Surgery, The First Affiliated Hospital of Zhengzhou University; 2The School of Basic Medical Science of Zhengzhou University, Zhengzhou, Henan 450052, P.

Effects of simvastatin on iNOS and caspase‑3 levels and oxidative stress following smoke inhalation injury.

The overexpression of inducible nitric oxide synthase (iNOS) induces cell apoptosis through various signal transduction pathways and aggravates lung injury. Caspase‑3 is an important protein in the apoptotic pathway and its activation can exacerbate apoptosis. Simvastatin, a hydroxymethyl glutaryl‑A reductase inhibitor, protects against smoke inhalation injury by inhibiting the synthesis and release of inflammatory factors and decreasing cell apoptosis.