Qunwei Lu

TL;DR: The hypothesis that Ca2+ desensitization of cardiac myofilament is the absolute cause of the pathogenesis of dilated cardiomyopathy associated with this mutation is verified and it is strongly suggested thatCa2+ sensitizers are beneficial for the treatment of Dilated carduomyopathy patients affected by sarcomeric regulatory protein mutations.

TL;DR: The effects of quercetin on the expression of Bmi‐1, a protein regulating mitochondrial function and ROS generation, is tested as a mechanism underlying quercETin‐mediated protection against doxorubicin‐induced cardiotoxicity.

TL;DR: MIONs were conjugated with the anti-cancer drug doxorubicin and its efficacy, as a model drug delivery system, was determined using HepG2 cells and the efficiency of the drug-NP conjugates was found to be significantly higher than that of the free drug (DOX).

TL;DR: It is suggested that R141W mutation in the strong tropomyosin-binding region of cardiac troponin T (cTnT) strengthens the integrity of cTnI in the thin filament by stabilizing the interaction between cTtnT and tropomyOSin, which might allow cTNI to inhibit thethin filament more effectively, leading to a Ca(2+) desensitization.

TL;DR: It is demonstrated that most of the HCM-linked cTnI mutations did affect the regulatory processes involving the cTNI molecule, and that at least five mutations increased the Ca(2+) sensitivity of cardiac muscle contraction.