Apelin-13 Activates TFEB-Mediated Autophagy Via AMPK To Attenuate Senescence And Pyroptosis In Nucleus Pulposus Cells During Intervertebral Disc Degeneration
Our spinal discs, which act as cushions between our vertebrae, can wear down over time, leading to a common and often painful condition called intervertebral disc degeneration. This degeneration is often linked to the aging of the cells within these discs, particularly the nucleus pulposus cells, which are crucial for disc health.
Scientists have been exploring why these cells fail, and two key culprits are impaired “autophagy” and increased “senescence” and “pyroptosis.” Autophagy is essentially the cell’s natural recycling system, clearing out damaged components to keep the cell healthy. When this system breaks down, cellular waste accumulates, contributing to disease. Senescence refers to cells getting old and dysfunctional, stopping their normal activities and sometimes releasing harmful substances. Pyroptosis is a highly inflammatory form of cell death that can worsen tissue damage.
A recent study has shed light on a promising solution: a naturally occurring peptide called Apelin-13. This peptide was found to effectively restore the cell’s recycling process in degenerating spinal disc cells. It does this by activating a key protein called TFEB, which acts like a master switch for genes involved in cellular cleanup, and helps it move into the cell’s control center, the nucleus.
Furthermore, Apelin-13 works through a cellular energy sensor pathway known as AMPK. By engaging this pathway, the peptide not only boosts the cell’s recycling capabilities but also significantly reduces both cellular aging and the inflammatory cell death process. In experiments using animal models, this treatment helped maintain the structure of the spinal discs and reduced the harmful signals associated with degeneration.
These findings suggest that targeting this pathway with Apelin-13 could be a novel and effective strategy for developing new treatments for intervertebral disc degeneration, potentially offering relief for millions suffering from chronic back pain.
Source: link to paper