FSTL1 accelerates nucleus pulposus-derived mesenchymal stem cell apoptosis in intervertebral disc degeneration by activating TGF-β-mediated Smad2/3 phosphorylation

Intervertebral disc degeneration (IVDD) is a major cause of low back pain. This study explores using nucleus pulposus-derived mesenchymal stem cells (NP-MSCs) to repair damaged discs. However, these cells don't always survive well in the harsh environment of a degenerated disc. The study found that a protein called FSTL1 increases in these cells in a degenerating disc. Increased FSTL1 seems to make the cells more likely to die and disrupts the materials that make up the disc. Blocking FSTL1 improved cell survival and disc health. The researchers also found that FSTL1 affects a signaling pathway called TGF-β/Smad2/3. This pathway is involved in cell growth and death. By blocking this pathway, they could partially reverse the harmful effects of FSTL1.

• 1
  FSTL1 expression is elevated in NP-MSCs from degenerated intervertebral discs in both humans and rats.
• 2
  Acidic conditions, mimicking the environment in a degenerating disc, upregulate FSTL1 expression in NP-MSCs.
• 3
  Silencing FSTL1 with siRNA reduced NP-MSC apoptosis and improved ECM anabolism, suggesting that FSTL1 plays a key role in accelerating NP-MSC apoptosis