Pharmacologic eigenvalues: beating the rap on bone marrow failure.
Patients suffering from sustained acute or chronic illness often have decreased white blood cell and platelet counts as well as anemia, and bone marrow studies routinely show only decreased numbers of blood precursor cells. While much has been recently learned about the cause of isolated anemia, the pathogenesis of true bone marrow failure (i.e., low bone marrow cellularity and low counts in multiple blood lineages) has remained elusive. In this issue of the JCI, Chen et al. present evidence that overactivation of mammalian target of rapamycin signaling in HSCs is found in two mouse models of bone marrow failure, and they show that treatment with rapamycin significantly normalizes the low blood counts.
Emerson
Stephen G
SG
Department of Biology, Haverford College, Haverford, Pennsylvania 19041, USA. semerson@haverford.edu
Garrett
Russell W
RW
D000740:Anemia / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D001853:Bone Marrow / Q000473:pathology / Q000503:physiopathology; D006410:Hematopoiesis / Q000276:immunology; D006412:Hematopoietic Stem Cells / Q000473:pathology / Q000502:physiology; D006801:Humans; D007113:Immunity, Innate; D007166:Immunosuppressive Agents / Q000627:therapeutic use; D036341:Intercellular Signaling Peptides and Proteins / Q000276:immunology; D051379:Mice; D009190:Myelodysplastic Syndromes / Q000188:drug therapy / Q000473:pathology* / Q000503:physiopathology*; D015398:Signal Transduction / Q000502:physiology; D020123:Sirolimus / Q000627:therapeutic use; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
D007166:Immunosuppressive Agents; D036341:Intercellular Signaling Peptides and Proteins; D014409:Tumor Necrosis Factor-alpha; D058570:TOR Serine-Threonine Kinases; D020123:Sirolimus