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Related Concept Videos

Bone Remodeling01:40

Bone Remodeling

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.
Bone Disorders01:29

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...
Bone Remodeling and Repair01:31

Bone Remodeling and Repair

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 bone...

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Related Experiment Video

Updated: Jul 5, 2026

A Rat Model of Pressure Overload Induced Moderate Remodeling and Systolic Dysfunction as Opposed to Overt Systolic Heart Failure
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Heart Failure but Not Myocardial Infarction Is Causing Bone Loss in Rodent Models in an FGF23-Independent Manner.

Svetlana Slavic1,2,3,4,5, Nejla Latic2, Norbert Hassler1

  • 1Ludwig Boltzmann Institute of Osteology, Heinrich-Collin-Strasse 30, 1140 Vienna, Austria.

International Journal of Molecular Sciences
|January 10, 2026
PubMed
Summary

Myocardial infarction (MI) and heart failure (HF) cause bone loss, but only HF induced by transverse aortic constriction (TAC) led to reduced bone mineral density (BMD) in mice, independently of FGF23.

Keywords:
bone mineral densityfibroblast growth factor-23heart failuremyocardial infarctionosteoporosistransverse aortic constriction

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Area of Science:

  • Cardiovascular Biology
  • Bone Metabolism
  • Translational Medicine

Background:

  • Myocardial infarction (MI) and heart failure (HF) are linked to decreased bone mineral density (BMD).
  • The direct causal relationship between cardiac injury and bone loss remains unclear.
  • Investigating specific cardiac conditions and their impact on bone is crucial for understanding comorbidities.

Purpose of the Study:

  • To determine if MI and HF directly induce bone loss.
  • To differentiate the skeletal effects of MI versus pressure-overload HF.
  • To explore the role of FGF23 in cardiac injury-induced bone changes.

Main Methods:

  • Induction of terminal MI in mice via coronary ligation.
  • Myocardial ischemia-reperfusion (I/R) injury in young and aged rats.
  • Transverse aortic constriction (TAC) in wild-type, Fgf23/VDR double mutant, and VDR-deficient mice.
  • Bone phenotyping using pQCT, histomorphometry, and biochemical analyses.

Main Results:

  • MI, in both terminal ischemia and I/R models, did not alter BMD in mice or rats.
  • TAC significantly reduced femoral cortical BMD in mice.
  • FGF23 deficiency did not prevent TAC-induced bone loss, indicating an FGF23-independent mechanism.

Conclusions:

  • Pressure-overload heart failure (HF) induced by TAC causes significant bone loss, particularly affecting cortical bone.
  • Myocardial infarction (MI) does not appear to directly cause bone loss in these models.
  • The bone loss associated with TAC-induced HF is independent of FGF23 signaling.