Key result
Deletion of both Plgf and eNos in mice subjected to hind-limb ischemia resulted in severe defective angiogenesis, with self-amputation and death occurring in up to 47% of the animals.
Why the study?
Does the combined deletion of Plgf and eNos worsen the vascular response and increase oxidative stress in mice with surgically induced hind-limb ischemia?
Does the combined deletion of Plgf and eNos worsen the vascular response and increase oxidative stress in mice with surgically induced hind-limb ischemia?
The combined deletion of PlGF and eNOS in mice exacerbates ischemic injury, highlighting their synergistic role in vascular response and tissue homeostasis during ischemia.
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Hypothesis-generating in mice; leaves open relevance of PlGF-eNOS synergy to human ischemic vascular disease.
Gigante et al. (2006) studied Surgically induced hind-limb ischemia. Plgf and eNos double knockout (Plgf-/- eNos-/-) vs. Plgf-/-, eNos-/-, and wild-type C57BL/6J mice was evaluated on Self-amputation and death. Deletion of both Plgf and eNos in mice subjected to hind-limb ischemia resulted in severe defective angiogenesis, with self-amputation and death occurring in up to 47% of the animals.
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