Researchers from the Chinese Academy of Sciences (CAS) have identified a key protein that exacerbates brain damage following an ischaemic stroke, offering a promising new target for future treatments.
Ischaemic stroke remains one of the leading causes of death and long-term disability worldwide. Although existing therapies can restore blood flow to the brain, many patients continue to suffer from secondary complications such as brain bleeding and impaired recovery. Until now, the molecular mechanisms behind this secondary injury have remained poorly understood.
In a study published in the European Heart Journal, scientists from the Shenzhen Institutes of Advanced Technology (SIAT) revealed that a protein known as DKK2 plays a critical role in worsening post-stroke brain damage. The researchers found that stressed neurons release elevated levels of DKK2 following a stroke.
Rather than protecting the brain, DKK2 suppresses an essential signaling pathway responsible for cell survival and maintaining blood vessel integrity. This interference weakens the blood–brain barrier, increasing the risk of hemorrhage and expanding the area of damaged brain tissue.
Experiments using mouse models showed that reducing DKK2 activity significantly limited brain injury and improved neurological recovery. In contrast, artificially increasing DKK2 levels led to more severe damage.
To validate their findings in humans, the researchers analyzed blood samples from stroke patients. They found that higher DKK2 levels were strongly associated with more extensive brain injury and poorer recovery outcomes after 90 days.
The discovery positions DKK2 as a potential therapeutic target for new stroke treatments. Modulating this protein could help protect brain tissue and reduce complications, particularly for patients who miss the narrow time window for current standard interventions.
