Osteopenia is caused by a lack of the HERC1 protein. Bones are constantly changing to keep them healthy. This process depends on the right balance between the activity of osteoclasts, which reabsorb bone tissue, and osteoblasts, which make bone tissue. An imbalance between these two can cause diseases like osteopenia, which is a loss of bone mass, and disrupt bone homeostasis.
The first evidence of the role of HERC1 protein in bone homeostasis is now provided by a study on model animals that was published in the journal Cell Death & Disease. The Bellvitge Biomedical Research Institute (IDIBELL) and the Cell Signaling and Bone Biology research group at the University of Barcelona carried out the study.
The study explains how the HERC1 deficiency stimulates both the activity of osteoblasts and osteoclasts, resulting in adult osteopenia and favoring bone reabsorption over bone formation.
According to the study’s findings, female mice with HERC1 deficiency are more likely to develop osteopenia in young mice, which is linked to lower testosterone and dihydrotestosterone levels.
RANKL and OPG proteins, which regulate the opposite of osteoclast differentiation and activation, are also produced by osteoblasts and osteocytes. The ratio of RANKL to OPG and the number of osteoclasts both rise as osteopenia brought on by HERC1 deficiency progresses. Based on these findings, RANKL is identified as a potential therapeutic target for people with bone disorders and HERC1 deficiency.
As per Jose Luis Rosa, teacher at the UB’s Staff of Medication and Wellbeing Sciences, top of the IDIBELL gathering and facilitator of the review, “the early identification of HERC1 variations with loss of capability could recognize people with inclination to create osteopenia and different pathologies connected with bone digestion, which could work on their therapy and clinical advancement.”
