Publications by authors named "Yingmei Lou"
Article Synopsis
- Researchers developed hpCas13d, an RNA nuclease, to effectively prevent hypertrophic cardiomyopathy in a specific mouse model, but further studies are needed for evaluating its long-term effects and safety.
- In a series of experiments, neonatal Myh6 mice were treated with AAV-hpCas13d, showing sustained absence of pathogenic Myh6 transcripts and improvements in heart function over 12 months without significant tissue damage or adverse immune reactions.
- These findings highlight the potential of AAV-hpCas13d as a viable gene therapy option for treating heart diseases, suggesting its readiness for further clinical application.
Atherosclerosis, characterized by the accumulation of lipid plaques on the inner walls of arteries, is the leading cause of heart attack, stroke and severe ischemic injuries. Senescent cells have been found to accumulate within atherosclerotic lesions and contribute to the progression of atherosclerosis. In our previous study, we discovered that suppressing Larp7 accelerates senescence by inhibiting Sirt1 activity, resulting in increased atherosclerosis in high-fat diet (HFD) fed and ApoE deficient (ApoE) mice.
View Article and Find Full Text PDFBackground: Familial hypertrophic cardiomyopathy has severe clinical complications of heart failure, arrhythmia, and sudden cardiac death. Heterozygous single nucleotide variants (SNVs) of sarcomere genes such as are the leading cause of this type of disease. CRISPR-Cas13 (clustered regularly interspaced short palindromic repeats and their associated protein 13) is an emerging gene therapy approach for treating genetic disorders, but its therapeutic potential in genetic cardiomyopathy remains unexplored.
View Article and Find Full Text PDFBackground: Heart failure (HF) is among the leading causes of morbidity and mortality, and its prevalence continues to rise. LARP7 (La ribonucleoprotein domain family member 7) is a master regulator that governs the DNA damage response and RNAPII (RNA polymerase II) pausing pathway, but its role in HF pathogenesis is incompletely understood.
Methods: We assessed LARP7 expression in human HF and in nonhuman primate and mouse HF models.