Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

Skeletal Aging and Osteoporosis: Cellular Senescence and Beyond

Version 1 : Received: 2 February 2021 / Approved: 3 February 2021 / Online: 3 February 2021 (17:00:00 CET)

How to cite: Chandra, A.; Rajawat, J. Skeletal Aging and Osteoporosis: Cellular Senescence and Beyond. Preprints 2021, 2021020127 (doi: 10.20944/preprints202102.0127.v1). Chandra, A.; Rajawat, J. Skeletal Aging and Osteoporosis: Cellular Senescence and Beyond. Preprints 2021, 2021020127 (doi: 10.20944/preprints202102.0127.v1).

Abstract

Bone is a dynamic organ maintained by tightly regulated mechanisms. With old age, bone homeostasis which is maintained by an intricate balance between bone formation and bone resorption, undergoes deregulation. Oxidative stress-induced DNA damage, cellular apoptosis, and cellular senescence are all responsible for this tissue dysfunction and the imbalance in bone homeostasis. These cellular mechanisms have become a target for therapeutics to treat age-related osteoporosis. Pharmacological and genetic mouse models have shown the importance of senescent cell clearance in alleviating age-related osteoporosis. Senescent cells have an altered secretome, which may have an autocrine, paracrine, or endocrine function. The current review discusses the current and potential pathways which lead to a senescence profile in an aged skeleton. The review was written following an extensive literature survey of published studies, mostly excluding articles published on pre-print servers. The review discusses potential therapeutics targeting cellular senescence and the senescent secretome as underlying pathogenesis of an aging bone.

Subject Areas

Osteoporosis; Senescence; SASP; Aging; Radiation; Senotherapeutic

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