Biweekly Research News Digest
This newsletter is designed to share with you research news in various fields where applications of gene sequencing can be found. It will share research findings from Novogene’s customers. By sharing insights from the most prestigious research teams, it is intended to call your attention to the latest applications of sequencing in life sciences and biomedical research and inspire your research.
We are pleased to reconnect with you in the Biweekly Research News Digest. In this week's featured articles, researchers utilize cutting-edge sequencing technologies, such as single-cell transcriptome sequencing and eukaryotic mRNA sequencing, to uncover insights into cardiac function, disease mechanisms, and potential therapies. These findings deepen our understanding of cardiac processes and open new avenues for treating heart conditions.
The Protective Role of DDX17 in Cardiac Function via the BCL6-DRP1 Pathway
DEAD-box helicase 17 (DDX17)?belongs to the DEAD-box family and functions as a transcriptional cofactor. It?is commonly found in the heart, but its exact function there remains unclear. According to a recent study published in Nature, researchers?explored the issue by?creating?cardiomyocyte-specific Ddx17-knockout (Ddx17-cKO) and Ddx17-transgenic (Ddx17-Tg) mice?and a variety of?heart failure (HF) and cardiomyocyte injury?models. They observed downregulation of DDX17 in heart failure and cardiomyocyte injury models and found that cardiomyocyte-specific knockout of Ddx17?resulted in progressive cardiac dysfunction, maladaptive remodeling and progression to heart failure. Conversely, restoring DDX17 expression protected cardiac function during disease states. The researchers also specified the mechanism in which reduction in DDX17 levels led to disrupted mitochondrial homeostasis, contributing to?heart failure.
Multi-Omics Analysis Reveals Potential Therapeutic Targets for Hypertrophic Cardiomyopathy
Hypertrophic cardiomyopathy (HCM) is a prevalent inherited heart disease characterized by left ventricular hypertrophy due to mutations in sarcomere genes. Researchers from Peking University and the Chinese Academy of Medical Science and Peking Union Medical College conducted a multi-omics analysis to investigate cardiac remodeling in HCM. Conducting NOMe-seq and RNA-seq of cardiac tissues from HCM patients, they found significant changes in gene expression, DNA methylation, and chromatin accessibility. In addition, targeting transcription factors SP1 and EGR1 in an HCM mouse model mitigated the HCM phenotype, suggesting a promising therapeutic strategy for HCM.
Histone Deacetylase 3's Role in Ventricular Trabeculation
Ventricular trabeculation failure is often linked to congenital heart disease.?Endocardial cell support is vital?for trabeculation. A collaborative research team?comprising researchers?from the United States and Germany explored endocardial cells’regulation of extracellular matrix and growth factor secretion. They observed early embryo lethality and ventricular hypotrabeculation?in histone deacetylase 3 (HDAC3) knockout mice, which, ?as shown by single-cell RNA sequencing, also led to?downregulated extracellular matrix components. They associated HDAC3 knockout?with lack of transforming growth factor ?3 (TGF-?3) ?and lower capacity in inducing?cardiomyocyte proliferation?and identified the pathway.?Their?findings provide insights into congenital heart disease and suggest potential strategies for myocardial regeneration.
Protective Role of Proline Dehydrogenase in Cardiac Remodeling: Potential Therapeutic Implications
Metabolic reprogramming plays a crucial role in pressure overload-induced cardiac remodeling. In a study recently published in Science Advances, scientists demonstrated that proline dehydrogenase (PRODH), a key enzyme in proline metabolism, plays a protective role against cardiac remodeling. They performed transverse aortic constriction (TAC) on both?cardiac-specific PRODH knockout and overexpression mice and?found that PRODH expression decreased?post-TAC.?Whereas the former group suffered from?worsened cardiac dysfunction, the latter group benefited from the protect effect of?overexpression.?These findings suggest that PRODH plays a modulating role in cardiac bioenergetics and redox homeostasis during the process of cardiac remodeling induced by pressure overload and underscore?its potential as a therapeutic target for cardiac remodeling.
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Role of Telomere Shortening in Cardiomyocyte Dysfunction and Senescence
Telomeres, located at the ends of chromosomes, are vital for aging and DNA damage response. Short telomeres are present in heart cells of individuals with genetic heart conditions, yet the role?of telomere lengths in cardiomyocyte?remains unclear. Researchers from Shanghai Jiao Tong University and Guangdong General Hospital investigated cardiomyocytes from heart failure patients?and found?telomeres?significantly shorter than those of?healthy individuals. They created isogenic human induced pluripotent stem cell derived cardiomyocytes (hiPSC-CMs) with both short and normal telomeres, finding that short telomeres led to cardiac dysfunction and increased senescence markers. Telomere shortening,?due to heightened chromatin accessibility, triggered FOXC1 expression. FOXC1 overexpression resulted in hiPSC-CM aging, mitochondrial and contractile dysfunction, which can be reversed by FOXC1?knockdown. This study underscores how telomere shortening influences chromatin accessibility and activates FOXC1-dependent pathways, contributing to contractile dysfunction and myocardial senescence.
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Novogene specializes in the application of advanced molecular biotechnology and high-performance computing in the research fields of life science and human health. Established in March 2011, Novogene strives to become a global leader in providing genetic science services and technology products. Novogene has set up operations and laboratories in the United States, the United Kingdom, Netherlands, Germany, as well as in China, Singapore and Japan.
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