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Related Concept Videos

Bone Disorders01:29

Bone Disorders

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Aging and its effect on bone remodeling is the most common cause of bone disorders. In young and healthy people, bone deposition and resorption happen at an equal rate to maintain optimal bone health.
Bone deposition is also affected by the levels of sex hormones like estrogen and testosterone that promote osteoblast activity and bone matrix synthesis. When the level of these hormones decreases due to aging, it causes a reduction in bone deposition. As a result, bone resorption by osteoclasts...
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The Effect of Aging on Tissues01:19

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Several body functions deteriorate with age. The external signs of aging are easily identifiable. For example, the skin becomes dry, less elastic, and thins out, forming wrinkles. The skin of the face begins to appear looser due to a decrease in the levels of elastic and collagen fibers in the connective tissue. Additionally, melanin production in the hair follicle decreases with age, resulting in gray hair. Moreover, the senses of sight and hearing decline, so glasses and hearing aids may...
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Aging01:26

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Aging is a complex biological phenomenon influenced by various processes that affect cellular and systemic functions. Several prominent theories attempt to explain its mechanisms, highlighting cellular limitations, oxidative damage, and hormonal changes as central factors in aging.
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Replicative Cell Senescence02:15

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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Mitochondria01:37

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Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
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Bone Remodeling01:40

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Bone remodeling is a continuous and balanced process of bone resorption by osteoclasts and bone formation by osteoblasts. In adults, it helps maintain bone mass and calcium homeostasis. While mechanical stress can stimulate turnover as part of the normal maintenance and reparative process, several hormones also regulate bone remodeling.
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Related Experiment Video

Updated: Nov 8, 2025

Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry
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Measurement of Protein Turnover Rates in Senescent and Non-Dividing Cultured Cells with Metabolic Labeling and Mass Spectrometry

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Bone Aging, Cellular Senescence, and Osteoporosis.

Robert J Pignolo1,2, Susan F Law1, Abhishek Chandra1,2

  • 1Department of Medicine Mayo Clinic Rochester MN USA.

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|April 19, 2021
PubMed
Summary
This summary is machine-generated.

Cellular senescence accumulation drives age-related osteoporosis by disrupting bone hemostasis. Clearing senescent cells or their secretory phenotype may offer therapeutic benefits for bone aging.

Keywords:
AGINGBONECELLULAR SENESCENCEOSTEOPOROSISSENOLYTICS

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Area of Science:

  • Gerontology
  • Bone Biology
  • Cellular Biology

Background:

  • Aging bone undergoes complex changes, including hormonal shifts, unloading, and cellular senescence, contributing to osteoporosis.
  • These age-related bone changes are exacerbated by medical conditions, medications, risk factors, and genetics.
  • Bone hemostasis and its age-related dysregulation are critical factors in osteoporosis development.

Purpose of the Study:

  • To summarize physiological changes in aging bone.
  • To review the role of cellular senescence in age-related osteoporosis.
  • To explore therapeutic strategies targeting senescent cells in bone aging.

Main Methods:

  • Review of major physiological changes in aging bone.
  • Summary of the role of cellular senescence in osteoporosis.
  • Analysis of senescence-associated secretory phenotype (SASP) in bone aging.
  • Examination of radiation-induced bone loss as a model for bone aging.

Main Results:

  • Cellular senescence accumulation in the bone microenvironment is a predominant mechanism for age-related osteoporosis.
  • Senescence-associated secretory phenotype (SASP) plays a significant role in bone aging.
  • Remodeling deficits and uncoupling phenomena contribute to bone loss with aging.

Conclusions:

  • Cellular senescence is a key driver of age-related osteoporosis.
  • Targeting senescent cells or their SASP presents a promising therapeutic avenue for bone aging.
  • Further research into senolytics and SASP inhibitors is warranted for osteoporosis treatment.