Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 218, Issue 7, Pages -Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20201544
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Funding
- NHLBI NIH HHS [R35 HL135787] Funding Source: Medline
- NIA NIH HHS [U01 AG077925, R01 AG069010] Funding Source: Medline
- NIDDK NIH HHS [R01 DK113639, R01 DK118072] Funding Source: Medline
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The aging population requires new therapeutic strategies to improve hematopoietic aging disorders; dysregulation of innate immune and inflammatory signaling leads to competitive advantage and clonal dominance; emerging concepts will reveal critical biology and therapeutic opportunities.
With a growing aged population, there is an imminent need to develop new therapeutic strategies to ameliorate disorders of hematopoietic aging, including clonal hematopoiesis and myelodysplastic syndrome (MDS). Cell-intrinsic dysregulation of innate immune-and inflammatory-related pathways as well as systemic inflammation have been implicated in hematopoietic defects associated with aging, clonal hematopoiesis, and MDS. Here, we review and discuss the role of dysregulated innate immune and inflammatory signaling that contribute to the competitive advantage and clonal dominance of preleukemic and MDS-derived hematopoietic cells. We also propose how emerging concepts will further reveal critical biology and novel therapeutic opportunities.
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