Venular-centered thrombo-inflammation drives microvascular failure after arterial recanalization in acute mesenteric ischemia
Abstract
BACKGROUND: Acute mesenteric ischemia (AMI) remains associated with high mortality despite prompt revascularization, suggesting that downstream ischemia-reperfusion injury contributes to poor outcomes. However, the microvascular mechanisms underlying this process are not entirely defined. METHODS: We analyzed admission blood samples from patients with arterial AMI and non-ischemic controls enrolled in the SURVIBIO diagnostic study (NCT03518099). We also investigated thrombo-inflammatory responses in a murine superior mesenteric artery occlusion (SMAO) model. In mice, intravital microscopy was used to directly visualize mesenteric microcirculatory flow and thrombo-inflammatory events during ischemia-reperfusion. RESULTS: Patients with AMI display a marked systemic thrombo-inflammatory profile, characterized by elevated inflammatory markers, neutrophil activation, platelet activation, and alterations in coagulation-related proteins, which are closely mirrored in the SMAO model. Intravital microscopy reveals a dissociation between arterial and microvascular reperfusion: while arteriolar flow partially recovers after recanalization, venular perfusion remains severely impaired and is associated with early blood cell stasis and stable venular thrombus formation. Thrombi develop through a sequential process initiated during ischemia and amplified during reperfusion. CONCLUSION: Together, these findings suggest that venular-centered thrombo-inflammation is closely associated with microvascular dysfunction and intestinal injury in arterial AMI. This work provides a framework for targeting thrombo-inflammatory pathways beyond arterial reperfusion that may extend to other clinical forms of AMI, including non-occlusive mesenteric ischemia (NOMI).
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BibTeX
@article{francois2026venularcentered,
title = {{Venular-centered thrombo-inflammation drives microvascular failure after arterial recanalization in acute mesenteric ischemia}},
author = {Déborah François and Lambert Kernanet and Melinda Bajul and Abigail Brami and Véronique Arocas and Marie-Christine Bouton and Dominique Cazals-Hatem and Kevin Guedj and Benoit Ho-Tin-Noé and Olivier Corcos and Yacine Boulaftali and Alexandre Nuzzo},
journal = {Communications Medicine},
year = {2026},
month = aug,
doi = {10.1038/s43856-026-01878-y},
url = {https://hal.science/hal-05790373v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Venular-centered thrombo-inflammation drives microvascular failure after arterial recanalization in acute mesenteric ischemia
AU - Déborah François
AU - Lambert Kernanet
AU - Melinda Bajul
AU - Abigail Brami
AU - Véronique Arocas
AU - Marie-Christine Bouton
AU - Dominique Cazals-Hatem
AU - Kevin Guedj
AU - Benoit Ho-Tin-Noé
AU - Olivier Corcos
AU - Yacine Boulaftali
AU - Alexandre Nuzzo
PY - 2026
DA - 2026/08/28
JO - Communications Medicine
DO - 10.1038/s43856-026-01878-y
UR - https://hal.science/hal-05790373v1
AB - BACKGROUND: Acute mesenteric ischemia (AMI) remains associated with high mortality despite prompt revascularization, suggesting that downstream ischemia-reperfusion injury contributes to poor outcomes. However, the microvascular mechanisms underlying this process are not entirely defined. METHODS: We analyzed admission blood samples from patients with arterial AMI and non-ischemic controls enrolled in the SURVIBIO diagnostic study (NCT03518099). We also investigated thrombo-inflammatory responses in a murine superior mesenteric artery occlusion (SMAO) model. In mice, intravital microscopy was used to directly visualize mesenteric microcirculatory flow and thrombo-inflammatory events during ischemia-reperfusion. RESULTS: Patients with AMI display a marked systemic thrombo-inflammatory profile, characterized by elevated inflammatory markers, neutrophil activation, platelet activation, and alterations in coagulation-related proteins, which are closely mirrored in the SMAO model. Intravital microscopy reveals a dissociation between arterial and microvascular reperfusion: while arteriolar flow partially recovers after recanalization, venular perfusion remains severely impaired and is associated with early blood cell stasis and stable venular thrombus formation. Thrombi develop through a sequential process initiated during ischemia and amplified during reperfusion. CONCLUSION: Together, these findings suggest that venular-centered thrombo-inflammation is closely associated with microvascular dysfunction and intestinal injury in arterial AMI. This work provides a framework for targeting thrombo-inflammatory pathways beyond arterial reperfusion that may extend to other clinical forms of AMI, including non-occlusive mesenteric ischemia (NOMI).
SN - 2730-664X
ER -