Key result
CCR2 and NR4A1 knockout impairs thrombus mass reduction in mice compared to wild-type.
Monocyte pathway disruption impairs murine thrombus resolution; hypothesis-generating for CTEPH persistence, with no clinical implications yet.
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Mohammed et al. (2026) studied Chronic thromboembolic pulmonary hypertension (CTEPH) (n=15). CCR2 and NR4A1 gene knockout vs. Wild-type (B6) mice was evaluated on Thrombus mass reduction from days 2 to 14 (p=<0.05). CCR2-knockout and NR4A1-knockout mice exhibited impaired thrombus mass reduction from days 2 to 14 compared to wild-type mice (33% and 47% vs 60%, respectively; P < .05).
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