Therapy-Induced Senescence Drives Bone Loss
نویسندگان
چکیده
منابع مشابه
Burn-induced Bone Loss
OBJECTIVE The purpose of this article is to familiarize the reader with the issue of bone loss that accompanies severe burn injury. Why is this important? How does it happen? How can we treat it? METHODS The published findings on this subject are reviewed and integrated into a conceptual framework. RESULTS Bone loss occurs quickly following a severe burn, is sustained, and increases the ris...
متن کاملRescuing Loading Induced Bone Formation at Senescence
The increasing incidence of osteoporosis worldwide requires anabolic treatments that are safe, effective, and, critically, inexpensive given the prevailing overburdened health care systems. While vigorous skeletal loading is anabolic and holds promise, deficits in mechanotransduction accrued with age markedly diminish the efficacy of readily complied, exercise-based strategies to combat osteopo...
متن کاملAndrogen Receptor Drives Cellular Senescence
The accepted androgen receptor (AR) role is to promote proliferation and survival of prostate epithelium and thus prostate cancer progression. While growth-inhibitory, tumor-suppressive AR effects have also been documented, the underlying mechanisms are poorly understood. Here, we for the first time link AR anti-cancer action with cell senescence in vitro and in vivo. First, AR-driven senescenc...
متن کاملReplication stress-induced endogenous DNA damage drives cellular senescence induced by a sub-lethal oxidative stress
Although oxidative stress has been shown to induce senescence and replication stress independently, no study has implicated unresolved replication stress as the driver for cellular senescence in response to oxidative stress. Using cells exposed to increasing concentrations of hydrogen peroxide, we show that sub-lethal amount of exogenous hydrogen peroxide induces two waves of DNA damage. The fi...
متن کاملSenescence induced by altered telomere state, not telomere loss.
Primary human cells in culture invariably stop dividing and enter a state of growth arrest called replicative senescence. This transition is induced by programmed telomere shortening, but the underlying mechanisms are unclear. Here, we report that overexpression of TRF2, a telomeric DNA binding protein, increased the rate of telomere shortening in primary cells without accelerating senescence. ...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Cancer Research
سال: 2020
ISSN: 0008-5472,1538-7445
DOI: 10.1158/0008-5472.can-19-2348