Key result
Cilostazol reduces post-stroke infarct volume in mice, driven by a ~31% increase in collateral flow.
Why the study?
There is a need to identify therapies capable of increasing collateral blood flow after stroke by repurposing FDA-approved drugs to induce collateral remodeling.
Does cilostazol improve collateral remodeling and reduce stroke severity in mice with acute middle cerebral artery obstruction?
Does cilostazol improve collateral remodeling and reduce stroke severity in mice with acute middle cerebral artery obstruction?
Cilostazol significantly increases collateral blood flow and reduces infarct volume in a mouse model of acute ischemic stroke, suggesting potential for repurposing in acute stroke management.
No takes yet. Share an insight, caveat, or question.
Should not yet change stroke practice; hypothesis-generating for cilostazol in human collateral remodeling.
The need to identify therapies capable of increasing collateral blood flow after stroke has recently come into focus. This study examined the idea of repurposing an already FDA-approved drug for a new indication—inducing collaterals to remodel to larger diameters after acute stroke. We tested cilostazol, an agent whose molecular mechanism of action suggested such a capability. Importantly, cilostazol is currently used to reduce the incidence of recurrent stroke and transient ischemic attack. In mice with abundant collaterals at baseline, 7-day administration of cilostazol at the dose used clinically beginning 2 h after obstruction of the MCA, boosted collateral growth, that is, anatomic lumen diameter, such that the increase in relative collateral flow post-stroke was augmented by 31% ( p = 0.004) 48 h after occlusion. The effect was stronger in mice with poor collaterals, 275% ( p = 0.018), in association with a significant decrease in infarct volume and improved functional outcome. Moreover, when combined with an experimental drug that acts by a complimentary mechanism vis-a-vis cilostazol, mice with poor collaterals experienced an additive 261% ( p = 0.007) additional increase 7 days post-occlusion. Cilostazol’s augmentation of remodeling extended to mice with advanced age or diabetes. This study provides a basis for further pre-clinical as well as clinical investigation.
Zhang et al. (2026) studied this question. Cilostazol increased collateral flow by 31% in mice after stroke and 275% in those with poor collaterals, reducing infarct volume significantly.
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