Blood: Targetbone myrita can save the impaired hematopoietic stem cell function of beta-thalassemia

Hematopoietic stem cells (HSCs) are regulated by signals from bone marrow (BM) niches, which regulate blood cell production in stable states and in blood diseasesTo understand the role of HSC-wall interactions in the steady state of non-malignant changes, the researchers chose a hemoglobin disease, beta-thalassemia, as an examplein this severe congenital anemia, secondary changes in primary hemoglobin defects have a potential effect on HSC-wall cross-linkingIn this study, the researchers found that hematopoietic stem cells in thalassemia mice (th3) suffered impaired function due to changes in the interaction of BM nichesThe self-renewal defect of HSC was repaired after transplantation to normal microenvironment, thus proving the positive effect of BM matrixConsistent with common findings of osteoporosis in patients, the researchers found that bone deposition decreased as levels of parathyroidism (PTH) decreased, and that parathyroidism (PTH) was not only a key regulatory factor for bone metabolism, but also an important regulatory factor for HSC activityin the body, activating the PTH signal by reconstructing Jagged1 and bone bridge protein levels is associated with saving th3 HSCs by correcting HSC-wallcrossIn patients with thalassemia, it was confirmed that the hSC of resting state decreased and that the characteristics of BM matrix niches changedthis study reveals HSCs defects caused by BM microenvironment changes in patients with beta-thalassemia, providing new insights into improved transplantation and gene therapy