Researchers have identified BRD4 as a new target for spinal disc degeneration, linking it to intervertebral disc degeneration (IDD) and its role in regulating gene expression.

In experiments with cells from IDD patients, it was demonstrated that BRD4 promotes senescence in nucleus pulposus (NP) cells, which correlates with the severity of IDD.

The study further revealed that the MAP2K7 gene, which is downstream of BRD4, contributes to cellular senescence and the degradation of the extracellular matrix (ECM) in NP cells.

Cellular senescence plays a significant role in IDD, with the senescence-associated secretory phenotype (SASP) degrading NP cells that are crucial for maintaining healthy spinal discs.

Intervertebral disc degeneration is a prevalent issue among the elderly, leading to reduced elasticity of discs and exacerbating back problems.

The signaling axis formed by BRD4, MAP2K7, and PGF has been identified as a key regulator of senescence and ECM maintenance, presenting potential drug targets for treatment.

These findings suggest that targeting the BRD4 signaling pathway could lead to effective treatments for age-related back pain and disc degeneration.

Manipulating levels of BRD4 and MAP2K7 showed that overexpression leads to increased senescence, while inhibition promotes ECM construction.

In a rat model, researchers observed that BRD4 levels increased as IDD progressed, further supporting its role in the degenerative process.

While previous studies have shown conflicting results regarding the STING pathway's role in IDD, this research shifts the focus to the involvement of BRD4.