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

Abstract

Hematopoiesis plays an essential role in supporting immune cell function and different physiological processes, such as nutrient transport, hemostasis, and would healing. In inflammatory scenarios, the typically stable state of hematopoiesis shifts to emergency myelopoiesis, generating necessary effector types of cell to address acute insults. Prolonged or unusual exposure of inflammatory signals adversely affects the hematopoiesis, causing enhanced proliferation, damage to DNA, and cell death such as necrosis, apoptosis, and pyroptosis. Additionally, the microenvironment of bone marrow undergoes alterations. Collectively, such variations can results in the early impairment of hematopoiesis. Particularly in patients having immune-mediated aplastic anemia or inherited bone marrow failure syndromes (BMFS), continuous exposure to inflammatory signals can worsen cytopenias and expedite the progression of disease. Nonetheless, the comprehension of specific characteristics of inflammation in bone marrow failure is understood poorly. 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.