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Cathepsin L and acute ischemic stroke: A mini-review
Linda Ma1, Silin Wu2, Aaron M Gusdon2
1Department of Neuroscience, Center for Basic and Translational Stroke Research, Rockefeller Neuroscience Institute, West Virginia University, Morgantown, WV, United States.
Frontiers in Stroke
|January 16, 2026
Summary
Cathepsin L, an enzyme, contributes to brain damage after ischemic stroke by degrading tissue. Inhibiting this enzyme reduced stroke severity and improved recovery, suggesting a potential therapeutic target.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Background:
- Ischemic stroke causes significant brain damage, including cell death and inflammation.
- Understanding molecular mechanisms is key to improving patient outcomes.
- Cathepsin L, a cysteine protease, is implicated in tissue degradation.
Purpose of the Study:
- To investigate the role of Cathepsin L in ischemic stroke.
- To determine if Cathepsin L contributes to brain tissue loss and inflammation post-stroke.
- To evaluate the therapeutic potential of Cathepsin L inhibition.
Main Methods:
- Immunohistochemical staining to detect Cathepsin L.
- Mass spectrometry to analyze protein and matrix degradation.
- Assessment of infarct size and functional scores after Cathepsin L inhibition.
Main Results:
- Cathepsin L levels increased in the ischemic core post-stroke.
- Elevated Cathepsin L correlated with extracellular matrix and perlecan degradation.
- Cathepsin L inhibition significantly reduced brain infarct size and improved functional outcomes.
Conclusions:
- Cathepsin L plays a significant role in post-stroke brain damage.
- Targeting Cathepsin L may offer a novel therapeutic strategy for ischemic stroke.
- Further research is needed to fully elucidate its role in inflammation and damage.
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