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Molecular Mechanisms Underlying an Aging Skeleton

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 13178

Special Issue Editor


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Guest Editor
Department of Physiology and Biomedical Engineering, Mayo Clinic College of Medicine, Rochester, MN 55905, USA
Interests: aging; DNA damage; apoptosis; cellular senescence; cancer; bone; bone marrow adiposity; osteoporosis; fracture; cancer treatments - chemotherapy and radiotherapy
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Special Issue Information

Dear Colleagues,

A Special Issue on the topic of “Molecular Mechanisms Underlying an Aging Skeleton” is being prepared for the journal IJMS. Bone is a dynamic organ that is under a balanced homeostasis during normal conditions. Aging, menopause in women, and several diseases tilt this balance, resulting in bone loss. Since bone is also an endocrine organ, changes in the bone environment may cause systemic changes. DNA damage, apoptosis, and cellular senescence together with a pro-inflammatory secretome drive age-related osteoporosis during normal physiological and pathological conditions. Molecular signatures that regulate these pathways in bone, and the autocrine, paracrine, or endocrine secretions that work locally and systemically are still being explored. This Special Issue will encompass studies that help us to understand these molecular signatures, focusing on cell fates to understand age- and disease-related bone loss. Several cellular events such as telomere shortening, epigenetic changes, proteostasis, mitochondrial dysfunction, and extracellular and intranuclear chromatin remodeling are all linked to cellular senescence. Research articles or reviews exploring the roles of these cellular mechanisms are solicited to understand the pathophysiology of an aging or diseased bone.

Dr. Abhishek Chandra
Guest Editor

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Keywords

  • DNA damage
  • cell death
  • cellular senescence
  • aging
  • osteoporosis
  • bone microenvironment

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Published Papers (1 paper)

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Review

25 pages, 1400 KiB  
Review
Skeletal Aging and Osteoporosis: Mechanisms and Therapeutics
by Abhishek Chandra and Jyotika Rajawat
Int. J. Mol. Sci. 2021, 22(7), 3553; https://doi.org/10.3390/ijms22073553 - 29 Mar 2021
Cited by 118 | Viewed by 12316
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 [...] Read more.
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 the bone homeostasis. These cellular mechanisms have become a target for therapeutics to treat age-related osteoporosis. Genetic mouse models have shown the importance of senescent cell clearance in alleviating age-related osteoporosis. Furthermore, we and others have shown that targeting cellular senescence pharmacologically was an effective tool to alleviate age- and radiation-induced osteoporosis. Senescent cells also have an altered secretome known as the senescence associated secretory phenotype (SASP), which may have autocrine, paracrine, or endocrine function. The current review discusses the current and potential pathways which lead to a senescence profile in an aged skeleton and how bone homeostasis is affected during age-related osteoporosis. The review has also discussed existing therapeutics for the treatment of osteoporosis and rationalizes for novel therapeutic options based on cellular senescence and the SASP as an underlying pathogenesis of an aging bone. Full article
(This article belongs to the Special Issue Molecular Mechanisms Underlying an Aging Skeleton)
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