Maternal hyperthyroidism and developing hematopoiesis dysfunction

What is it about?

The genomic and non-genomic actions of THs may regulate the developmental hematopoiesis system (cell proliferation and growth, and cell cycle), the RBCs, WBCs, and platelet counts. Maternal hyperthyroidism may disrupt the genomic and non-genomic mechanisms of THs. Maternal hyperthyroidism may cause dysfunction in the developing hematopoietic system because of THs can induce the production of the hematopoietic cell in the bone marrow. Future works are desired to overview the defects of maternal hyperthyroidism on the physiological (RBCs, WBCs, and platelet counts, and thrombocytopoiesis) and developmental hematopoiesis (hematopoietic stem cell proliferation and growth, cell cycle and apoptosis) in experimental animals and humans. Specifically, the additional studies are required to investigate the significant roles of THs in controlling the development of leukopoiesis, erythropoiesis, and hematopoietic lineages. This may benefit to increase our consideration of the interactions between THs and hematopoiesis during the development and suggest new therapeutic interferences in thyroid disorders. These arguments need more examination.

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Why is it important?

Maternal hyperthyroidism may disrupt the genomic and non-genomic mechanisms of THs. Maternal hyperthyroidism may cause dysfunction in the developing hematopoietic system because of THs can induce the production of the hematopoietic cell in the bone marrow.

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