Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

The Effect of Aging on Tissues

The Effect of Aging on Tissues

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...

Bone Disorders

Bone Disorders

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...

The Functions of the Skeletal System

The Functions of the Skeletal System

The most apparent functions of the skeletal system are support, protection, and movement. However, bone tissue also performs several other critical metabolic functions. For one, the bone matrix acts as a reservoir for a number of minerals important to the functioning of the body, especially calcium and phosphorus. These minerals, present in the bone tissue, can be released back into the bloodstream when required. Calcium ions, for example, are essential for muscle contractions and controlling...

Cellular Adaptation I: Introduction and Atrophy

Cellular Adaptation I: Introduction and Atrophy

Cells can adapt to environmental changes to maintain function and avoid injury, a process called cellular adaptation. Adapted cells exist in a reversible intermediate state with changes in size, number, phenotype, metabolism, or function. These responses help cells meet altered physiological or pathological demands; for example, enlargement of breast and uterine tissues during pregnancy. Early adaptations may enhance function, but persistent stress eventually causes tissue damage.Types of...

Changes in the Appendicular Skeleton with Age

Changes in the Appendicular Skeleton with Age

The upper and lower limb initially develops as a small bulge called a limb bud, which appears on the lateral side of the early embryo. The upper limb bud appears near the end of the fourth week of development, with the lower limb bud appearing shortly after.
Initially, the limb buds consist of a core of mesenchyme covered by a layer of ectoderm. The ectoderm at the end of the limb bud thickens to form a narrow crest called the apical ectodermal ridge. This ridge stimulates the underlying...

Regulation of Hematopoietic Stem Cells

Regulation of Hematopoietic Stem Cells

All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Protocol for standardized minimally invasive mouse models of bisphosphonate-related and radiation-induced jaw osteonecrosis.

bioRxiv : the preprint server for biology·2026

Same author

MicroRNA networks associated with skeletal aging and WNT pathway modulation.

Calcified tissue international·2026

Same author

Ultrasound imaging of small peripheral nerves - a primer for radiologists.

Journal of ultrasonography·2026

Same author

Complete Heart Block Related to Bicuspid Aortic Valve Calcification in a Triathlete.

JACC. Case reports·2026

Same author

Primary Cilia Are Required for Efficient BMP Signaling in Traumatic Heterotopic Ossification.

Biomedicines·2026

Same author

Suppression of early pro-inflammatory senescent signature post-radiotherapy mitigates chronic bone damage.

bioRxiv : the preprint server for biology·2026

Search research articles

Related Experiment Video

Updated: May 26, 2026

Stromal Cell Isolation From Hematopoietic Organs

Stromal Cell Isolation From Hematopoietic Organs

Published on: January 26, 2024

Bone Marrow Skeletal Stem Cell Dysfunction: Adipocytes during skeletal aging and senescence.

Aqsa Komel^1,2, David Achudhan^1,2, Abhishek Chandra^1,2,3

¹Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, Minnesota, USA.

Current Opinion in Endocrine and Metabolic Research

|May 25, 2026

Summary

Cellular senescence drives skeletal stem cells (SSCs) to become bone marrow adipocytes (BMAd), increasing bone resorption. Clearing senescent cells may offer therapeutic strategies against BMAd and bone loss.

Keywords:

Aging BMAT bone marrow adiposity senescence stem cell dysfunction

More Related Videos

Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans

Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans

Published on: February 16, 2017

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Related Experiment Videos

Last Updated: May 26, 2026

Stromal Cell Isolation From Hematopoietic Organs

Stromal Cell Isolation From Hematopoietic Organs

Published on: January 26, 2024

Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans

Preparation and Culture of Myogenic Precursor Cells/Primary Myoblasts from Skeletal Muscle of Adult and Aged Humans

Published on: February 16, 2017

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Area of Science:

Biomedical Science
Cell Biology
Stem Cell Research

Background:

Skeletal stem cells (SSCs) differentiate into various bone cells, but their fate can be skewed towards bone marrow adipocytes (BMAd).
This skewing contributes to increased bone resorption and altered bone accrual, impacting bone health in physiological and pathological states.
Cellular senescence, characterized by DNA damage and reactive oxygen species, is a key molecular pathway influencing SSC fate.

Purpose of the Study:

To review the direct and indirect roles of cellular senescence in the bone marrow environment.
To discuss how senescence influences SSC differentiation into BMAd.
To explore therapeutic potential of targeting senescent cells for bone loss.

Main Methods:

Literature review of preclinical studies on cellular senescence and SSC differentiation.
Analysis of molecular pathways involved in SSC fate regulation.
Examination of studies involving pharmacological and genetic clearance of senescent cells.

Main Results:

Cellular senescence directly and indirectly promotes SSC differentiation into BMAd.
Senescence-associated proinflammatory factors contribute to this altered cell fate.
Preclinical evidence supports the clearance of senescent cells as a viable strategy.

Conclusions:

Cellular senescence is a critical regulator of SSC fate, promoting adipogenesis over osteogenesis.
Targeting senescent cells and their associated inflammatory signatures presents a promising therapeutic avenue.
Mitigating BMAd accumulation through senolytic therapies could help preserve bone mass and reduce bone loss.