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Related Concept Videos

Bone Disorders01:29

Bone Disorders

5.0K
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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Bone Remodeling01:40

Bone Remodeling

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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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The Effect of Aging on Tissues01:19

The Effect of Aging on Tissues

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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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Hormones and Bone Tissue01:17

Hormones and Bone Tissue

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The endocrine system produces and secretes hormones, which interact with the skeletal system. These hormones control bone growth, maintain bone once it is formed, and remodel it.
Hormones That Influence Osteoblasts and/or Maintain the Matrix
Several hormones are necessary for controlling bone growth and maintaining the bone matrix. The pituitary gland secretes growth hormone (GH), which, as its name implies, controls bone growth. This happens in several ways: first, it triggers chondrocyte...
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Osteoclasts in Bone Remodeling01:31

Osteoclasts in Bone Remodeling

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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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Updated: Dec 31, 2025

Estrogen-Like Effect of Bazi Bushen Capsule in Ovariectomized Rats
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Therapy-Induced Senescence Drives Bone Loss.

Zhangting Yao1, Bhavna Murali1, Qihao Ren1

  • 1Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri.

Cancer Research
|January 15, 2020
PubMed
Summary

Senescent cells drive chemotherapy-induced bone loss through a senescence-associated secretory phenotype. Targeting the p38MAPK-MK2 pathway with inhibitors can preserve bone integrity and improve cancer survivor quality of life.

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Area of Science:

  • Oncology
  • Gerontology
  • Bone Biology

Background:

  • Chemotherapy is crucial for cancer treatment but causes toxicities, including long-term bone loss.
  • While estrogen loss is implicated, evidence suggests estrogen-independent mechanisms contribute to chemotherapy-induced bone loss.

Purpose of the Study:

  • To investigate the role of cellular senescence and its secretory phenotype in chemotherapy-induced bone loss.
  • To identify potential therapeutic targets for preventing bone loss in cancer survivors.

Main Methods:

  • Utilized clinically relevant mouse models of chemotherapy treatment.
  • Assessed the impact of senescent cell depletion and p38MAPK-MK2 pathway inhibition on bone integrity.

Main Results:

  • Cellular senescence and its senescence-associated secretory phenotype (SASP) were identified as key drivers of chemotherapy-induced bone loss.
  • Depleting senescent cells or inhibiting the p38MAPK-MK2 pathway preserved bone integrity in treated mice.

Conclusions:

  • Senescent cells are major contributors to chemotherapy-induced bone loss via SASP.
  • The p38MAPK-MK2 pathway represents a promising therapeutic target to prevent bone loss and enhance cancer survivor quality of life.