Aging and lineage allocation changes of bone marrow skeletal (stromal) stem cells
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Aging and lineage allocation changes of bone marrow skeletal (stromal) stem cells. / Nehlin, Jan O.; Jafari, Abbas; Tencerova, Michaela; Kassem, Moustapha.
I: Bone, Bind 123, 2019, s. 265-273.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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TY - JOUR
T1 - Aging and lineage allocation changes of bone marrow skeletal (stromal) stem cells
AU - Nehlin, Jan O.
AU - Jafari, Abbas
AU - Tencerova, Michaela
AU - Kassem, Moustapha
PY - 2019
Y1 - 2019
N2 - Aging is associated with decreased bone mass and accumulation of bone marrow adipocytes. Both bone forming osteoblastic cells and bone marrow adipocytes are derived from a stem cell population within the bone marrow stroma called bone marrow stromal (skeletal or mesenchymal) stem cells (BMSC). In the present review, we provide an overview, based on the current literature, regarding the physiological aging processes that cause changes in BMSC lineage allocation, enhancement of adipocyte and defective osteoblast differentiation, leading to gradual exhaustion of stem cell regenerative potential and defects in bone tissue homeostasis and metabolism. We discuss strategies to preserve the “youthful” state of BMSC, to reduce bone marrow age-associated adiposity, and to counteract the overall negative effects of aging on bone tissues with the aim of decreasing bone fragility and risk of fractures.
AB - Aging is associated with decreased bone mass and accumulation of bone marrow adipocytes. Both bone forming osteoblastic cells and bone marrow adipocytes are derived from a stem cell population within the bone marrow stroma called bone marrow stromal (skeletal or mesenchymal) stem cells (BMSC). In the present review, we provide an overview, based on the current literature, regarding the physiological aging processes that cause changes in BMSC lineage allocation, enhancement of adipocyte and defective osteoblast differentiation, leading to gradual exhaustion of stem cell regenerative potential and defects in bone tissue homeostasis and metabolism. We discuss strategies to preserve the “youthful” state of BMSC, to reduce bone marrow age-associated adiposity, and to counteract the overall negative effects of aging on bone tissues with the aim of decreasing bone fragility and risk of fractures.
KW - Adiposity
KW - Aging
KW - Bone marrow stromal stem cells
KW - Senescence
KW - Signaling pathways
U2 - 10.1016/j.bone.2019.03.041
DO - 10.1016/j.bone.2019.03.041
M3 - Journal article
C2 - 30946971
AN - SCOPUS:85064173743
VL - 123
SP - 265
EP - 273
JO - Bone
JF - Bone
SN - 8756-3282
ER -
ID: 216871064