About this Research Topic
The differentiation of progenitor and stem cells into different cell types is essential in the development of organs. While maintaining normal cellular differentiation is a necessity, any abnormality in these cellular and molecular pathways contributes to disease pathogenesis which can carry lethal consequences. In order to address the disease, the cause and type of pathogenesis must be identified. Genetics, epigenetics and external factors including invading pathogens can induce malfunction of the intra- and inter-cellular events.
Genetically inherited diseases are numerous and are carried through the differentiation pathways of stem or progenitor cells to the altered functional phenotypes. Abnormal genetic inheritance can also affect the cellular differentiation processes causing abnormal levels or lack of certain differentiated cells and their associated molecular and cellular functions. Epigenetic changes can also be the cause of cellular disorders such as single cell type- or pan-cytopenias. Similarly, deficiency of endothelial cells can affect both the formation of multipotent hematopoietic progenitors and the angioblasts that differentiate into multi-potent mesenchymal stem cells and the unipotent endothelial progenitor cells. Dysfunctions of stem or progenitor cells therefore originate from either genetic inheritance, or epigenetic consequences due to an acquired disorder or disease.
A lack of normal and sufficient renewable progenitor cells to maintain homeostasis can result in devastating consequences including haematological and endothelial defects that otherwise maintain normal blood and vessel formation respectively, triggering cytopenias or malignancies and hampering vasculogenesis and angiogenesis, the latter promoting atherosclerosis.
It is essential to understand the mechanisms of molecular pathways that make cells function. Investigations into the onset of disease pathogenesis due to endogenous molecular genetics or exogenous agents such as viruses and other pathogens affecting the functions of different cellular types in a diverse manner is a necessity. The intricacy of cellular dysfunctions created by the invading pathogen for example, is expected to be more complex at a stage where the cells, such as the progenitor cells are yet to differentiate, whereby they would express mature phenotypes and be specific to the appropriate organs. The nature and causes of genetic and epigenetic functions and disruptions of the mechanisms at molecular and cellular levels, which affect organ formation or malfunction are yet to be fully understood. Development of protocols for therapeutic corrections and treatments to maintain or re-attain normal cellular functions for alleviation of disease pathogenesis is also a priority.
In this Research Topic we welcome articles that focus on but are not limited to:
• Genetic predisposition as a cause in disease pathogenesis since this etiology stems from phenotypic gene expression and functional changes occurring at the molecular and cellular levels.
• Genomic defects that affect the molecular mechanisms of cellular functions with consequences to altered cell differentiation patterns.
• Abnormal cellular events acquired by epigenetic germ cell development through parental transfer to the progeny.
• Recent advances in the diverse sub/disciplines of biomedical sciences and biomedicine which begin to allow us to make changes to the genetic makeup of the organisms and hence restore normal functions, when altered post-fertilization in undifferentiated progenitor stem cells, in a cycle of events including the reversal to primordial germ cells.
• Embryonic or induced pluripotent stem cells generated from somatic cell nuclei transfer or reprogramming respectively, that may also participate in the germ cell formation.
• Visualization of molecular changes at the single-cell level for realizing causes of abnormal cellular functions and the means to alleviate potential disease pathogenesis.
• Investigations into mechanisms and corrective measures of cellular functions that affect vasculogenesis and angiogenesis responsible for haematological and endothelial dysfunctions.
• Immunological therapies for abnormal angiogenesis including tumorigenesis.
• High-throughput analyses performed on a micro level to detect single cell intracellular molecular variations including proteomics.
• Simulations of changes of different organ mechanisms and functions as evaluated using organoid models.
Genetically inherited diseases are numerous and are carried through the differentiation pathways of stem or progenitor cells to the altered functional phenotypes. Abnormal genetic inheritance can also affect the cellular differentiation processes causing abnormal levels or lack of certain differentiated cells and their associated molecular and cellular functions. Epigenetic changes can also be the cause of cellular disorders such as single cell type- or pan-cytopenias. Similarly, deficiency of endothelial cells can affect both the formation of multipotent hematopoietic progenitors and the angioblasts that differentiate into multi-potent mesenchymal stem cells and the unipotent endothelial progenitor cells. Dysfunctions of stem or progenitor cells therefore originate from either genetic inheritance, or epigenetic consequences due to an acquired disorder or disease.
A lack of normal and sufficient renewable progenitor cells to maintain homeostasis can result in devastating consequences including haematological and endothelial defects that otherwise maintain normal blood and vessel formation respectively, triggering cytopenias or malignancies and hampering vasculogenesis and angiogenesis, the latter promoting atherosclerosis.
It is essential to understand the mechanisms of molecular pathways that make cells function. Investigations into the onset of disease pathogenesis due to endogenous molecular genetics or exogenous agents such as viruses and other pathogens affecting the functions of different cellular types in a diverse manner is a necessity. The intricacy of cellular dysfunctions created by the invading pathogen for example, is expected to be more complex at a stage where the cells, such as the progenitor cells are yet to differentiate, whereby they would express mature phenotypes and be specific to the appropriate organs. The nature and causes of genetic and epigenetic functions and disruptions of the mechanisms at molecular and cellular levels, which affect organ formation or malfunction are yet to be fully understood. Development of protocols for therapeutic corrections and treatments to maintain or re-attain normal cellular functions for alleviation of disease pathogenesis is also a priority.
In this Research Topic we welcome articles that focus on but are not limited to:
• Genetic predisposition as a cause in disease pathogenesis since this etiology stems from phenotypic gene expression and functional changes occurring at the molecular and cellular levels.
• Genomic defects that affect the molecular mechanisms of cellular functions with consequences to altered cell differentiation patterns.
• Abnormal cellular events acquired by epigenetic germ cell development through parental transfer to the progeny.
• Recent advances in the diverse sub/disciplines of biomedical sciences and biomedicine which begin to allow us to make changes to the genetic makeup of the organisms and hence restore normal functions, when altered post-fertilization in undifferentiated progenitor stem cells, in a cycle of events including the reversal to primordial germ cells.
• Embryonic or induced pluripotent stem cells generated from somatic cell nuclei transfer or reprogramming respectively, that may also participate in the germ cell formation.
• Visualization of molecular changes at the single-cell level for realizing causes of abnormal cellular functions and the means to alleviate potential disease pathogenesis.
• Investigations into mechanisms and corrective measures of cellular functions that affect vasculogenesis and angiogenesis responsible for haematological and endothelial dysfunctions.
• Immunological therapies for abnormal angiogenesis including tumorigenesis.
• High-throughput analyses performed on a micro level to detect single cell intracellular molecular variations including proteomics.
• Simulations of changes of different organ mechanisms and functions as evaluated using organoid models.
Keywords: Disease, Differentiation, Endothelium, Epithelium, Hematopoiesis, Atherosclerosis, Cellular Antigens, Cell Cycle, Virus Infection, Organoid, Cell Signaling, High-Throughput Screening, Gene Editing, Single-Cell Proteomics, Epigenetics
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