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Clonal Haematopoiesis of Indeterminate potential and Cardiovascular diseases : A review.
Indian Heart J
January 2025
Department of Cardiology, Sri Ramachandra Institute of Higher Education & Research (SRIHER), Chennai, INDIA.
Cardiovascular disease (CVD) is a major driver of mortality and declining health worldwide. Cardiovascular diseases (CVD) is the most common cause of morbidity and mortality globally. Although dyslipidemia, smoking, diabetes, hypertension and obesity are some well-known causes of CVD, the overlapping genetic pathways between other diseases and those affecting cardiovascular health have been overlooked.
View Article and Find Full Text PDFRNase T2 deficiency promotes TLR13-dependent replenishment of tissue-protective Kupffer cells.
J Exp Med
March 2025
Division of Innate Immunity, The Institute of Medical Science, The University of Tokyo, Minato-ku, Japan.
Lysosomal stress due to the accumulation of nucleic acids (NAs) activates endosomal TLRs in macrophages. Here, we show that lysosomal RNA stress, caused by the lack of RNase T2, induces macrophage accumulation in multiple organs such as the spleen and liver through TLR13 activation by microbiota-derived ribosomal RNAs. TLR13 triggered emergency myelopoiesis, increasing the number of myeloid progenitors in the bone marrow and spleen.
View Article and Find Full Text PDFExploring Epigenetic Complexity in Regulation of Hematopoietic Stem Cells Niche: A Mechanistic Journey from Normal to Malignant Hematopoiesis.
Adv Exp Med Biol
January 2025
Centre for Diagnostic, Therapeutic and Investigative Studies, Faculty of Health Sciences, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia.
Epigenetic regulation in hematopoietic stem cells (HSCs) research has emerged as a transformative molecular approach that enhances understanding of hematopoiesis and hematological disorders. This chapter investigates the intricate epigenetic mechanisms that control HSCs function, including deoxyribonucleic acid (DNA) methylation, histone modifications, and chromatin remodeling. It also explores the role of non-coding ribonucleic acid (RNAs) as epigenetic regulators, highlighting how changes in gene expression can occur without alterations to the DNA sequence.
View Article and Find Full Text PDFInvestigating resistance to 5-Azacytidine and Venetoclax in PDX models of MDS/AML.
Front Oncol
January 2025
BIOCEV, First Faculty of Medicine, Charles University, Prague, Czechia.
Introduction: Progressing myelodysplastic syndrome (MDS) into acute myeloid leukemia (AML) is an indication for hypomethylating therapy (HMA, 5-Azacytidine (AZA)) and a BCL2 inhibitor (Venetoclax, VEN) for intensive chemotherapy ineligible patients. Mouse models that engraft primary AML samples may further advance VEN + AZA resistance research.
Methods: We generated a set of transplantable murine PDX models from MDS/AML patients who developed resistance to VEN + AZA and compared the differences in hematopoiesis of the PDX models with primary bone marrow samples at the genetic level.
An orally available P1'-5-fluorinated M inhibitor blocks SARS-CoV-2 replication without booster and exhibits high genetic barrier.
PNAS Nexus
January 2025
Department of Refractory Viral Diseases, National Center for Global Health and Medicine Research Institute, 1-21-1 Toyama, Shinjuku-ku, Tokyo 162-8655, Japan.
We identified a 5-fluoro-benzothiazole-containing small molecule, TKB272, through fluorine-scanning of the benzothiazole moiety, which more potently inhibits the enzymatic activity of SARS-CoV-2's main protease (M) and more effectively blocks the infectivity and replication of all SARS-CoV-2 strains examined including Omicron variants such as SARS-CoV-2 and SARS-CoV-2 than two M inhibitors: nirmatrelvir and ensitrelvir. Notably, the administration of ritonavir-boosted nirmatrelvir and ensitrelvir causes drug-drug interactions warranting cautions due to their CYP3A4 inhibition, thereby limiting their clinical utility. When orally administered, TKB272 blocked SARS-CoV-2 replication without ritonavir in B6.
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