From Inflammatory Cascades to Hematopoietic Consequences: A Review of Bone Marrow Failure Mechanisms

Abstract

Hematopoiesis plays a crucial role in supporting immune cell function and various physiological processes, including nutrient transport, hemostasis, and would healing. In the presence of inflammatory conditions, the typically stable state of hematopoiesis shifts to emergency myelopoiesis, generating effector cell types necessary to address acute insults. Prolonged or aberrant exposure to inflammatory signals adversely affects the hematopoietic system, leading to increased proliferation, DNA damage, and various forms of cell death such as apoptosis, pyroptosis, and necroptosis. Additionally, the bone marrow microenvironment undergoes modifications. Collectively, these changes can results in the premature impairment of hematopoietic function. Particularly in individuals with inherited bone marrow failure syndromes or immune – mediated aplasic anemia, continuous exposure to inflammatory signals may worsen cytopenias and expedite disease progression. Nonetheless, the comprehension of the specific roles of inflammation in bone marrow failure remains limited. This review synthesizes findings from diverse mouse models exploring inflammatory mechanisms in bone marrow failure and delves into their implications for prospective research and clinical applications.