98%
921
2 minutes
20
[This corrects the article DOI: 10.3389/fonc.2022.895708.].
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12321222 | PMC |
http://dx.doi.org/10.3389/fonc.2025.1641207 | DOI Listing |
Front Oncol
July 2025
Kunming College of Life Science, University of Chinese Academy of Sciences, Beijing, China.
[This corrects the article DOI: 10.3389/fonc.2022.
View Article and Find Full Text PDFJ Mol Cell Cardiol Plus
June 2025
Cardiovascular Medicine Section and Myocardial Biology Unit, and the Clinical and Translational Institute, Boston University School of Medicine, Boston, MA, United States of America.
Background: Mitochondrial dysfunction with decreased ATP production and increased release of reactive oxygen species (ROS) is a hallmark of the failing heart. Although SGLT2 inhibitors have been shown to improve myocardial metabolism in the failing heart, independent of diabetes, the effect on mitochondria is not clear.
Objectives: Our goal was to test the effect of the SGLT2 inhibitor ertugliflozin on mitochondrial gene expression and function in myocardium and isolated mitochondria from non-diabetic mice with dilated cardiomyopathy due to cardiac-specific over-expression of Gαq.
Brain
April 2025
F.M. Kirby Neurobiology Center, Boston Children's Hospital, Boston, MA, 02115, USA.
Inherited erythromelalgia, small fiber neuropathy and paroxysmal extreme pain disorder are caused by gain-of-function mutations in the voltage gated sodium channel Nav1.7. How different mutations in the same channel enhancing electrogenesis in sensory neurons results in such distinct disease presentations remains unknown.
View Article and Find Full Text PDFSci Rep
February 2025
Department of Laboratory Medicine, Division of Microbiology, Immunology and Glycobiology, Lund University, Klinikgatan 28, Lund, 221 84, Sweden.
Identifying specific inhibitors of the MYC oncogene has been challenging, due to off target effects associated with MYC inhibition. This study investigated how the recombinant Escherichia coli Lon protease (rLon), which targets MYC in human cells, inhibits MYC over-activation in models of infection and cancer. In silico predictions identified specific peptide domains of bacterial Lon that target MYC and the affinity of these peptides for MYC was investigated by surface plasmon resonance.
View Article and Find Full Text PDFNat Prod Res
December 2024
Department of Pharmacology and Toxicology, College of Pharmacy, Prince Sattam bin Abdulaziz University, Al-Kharj, Saudi Arabia.