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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.
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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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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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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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Osteoclasts are cells responsible for bone resorption and remodeling. They originate from hematopoietic progenitor cells present in the bone marrow. Numerous progenitor cells fuse to form multinucleated cells, each with 10-20 nuclei. A single osteoclast has a diameter of 150 to 200 µM. These cells have ruffled borders that break down the underlying bone tissue and release minerals such as calcium into the blood in bone resorption. Osteoclasts cling to bones with their ruffled edges during...
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Insights into age-related osteoporosis from senescence-based preclinical models and human accelerated aging

Robert J Pignolo1, Abhishek Chandra2

  • 1Department of Medicine, Divisions of Geriatric Medicine and Gerontology, Endocrinology, and Hospital Internal Medicine, the Department of Physiology and Biomedical Engineering, and the Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, United States.

Mechanisms of Ageing and Development
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This summary is machine-generated.

Cellular senescence and its secretory phenotype drive age-related bone loss and osteoporosis. Targeting senescent cells offers a potential therapeutic strategy for osteoporosis.

Keywords:
Accelerated agingAnimal modelsCellular senescenceOsteoporosisRadiationTelomerase dysfunction

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Area of Science:

  • Gerontology
  • Bone Biology
  • Cellular Senescence

Background:

  • Age-related osteoporosis is a significant health concern.
  • Cellular senescence, characterized by the senescence-associated secretory phenotype (SASP), is increasingly implicated in aging processes.
  • Mitochondrial dysfunction is linked to senescence and age-related diseases like osteoporosis.

Purpose of the Study:

  • To review preclinical models of age-related osteoporosis.
  • To explore the role of cellular senescence and SASP in bone loss.
  • To investigate the contribution of mitochondrial dysfunction and non-genetic aging paradigms to osteoporosis.

Main Methods:

  • Utilized preclinical animal models (telomere dysfunction, radiation, genetic/pharmacological senescent cell targeting).
  • Examined mitochondrial dysfunction via mtDNA polymerase gamma (Polg) gene mutations in mice.
  • Evaluated non-genetic human accelerated aging syndromes (skeletal unloading, premature ovarian failure, childhood cancer survivors).

Main Results:

  • Preclinical models support a key role for cellular senescence and SASP in aging-onset bone loss.
  • SASP mediates detrimental local and systemic skeletal effects.
  • Mitochondrial dysfunction and non-genetic aging syndromes highlight pathways like adipogenic lineage switching, Wnt inhibition, and increased osteoclastogenesis in senile osteoporosis.

Conclusions:

  • Cellular senescence is a critical driver of age-related bone loss.
  • Targeting senescent cells and their SASP is a promising therapeutic avenue for osteoporosis.
  • Understanding non-genetic aging syndromes provides insights into senile osteoporosis mechanisms.