Current molecular medicine · 2026
Effect of Renal Artery Stenosis on Hind Limb Perfusion and Arteriogenesis After Left Femoral Artery Ligation in Rats: E-RASHEF Study.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Zheng Bin
Аннотация
BACKGROUND/OBJECTIVE: Patients with renal artery stenosis (RAS) exhibit increased risk of cardiovascular death and all-cause death. Our previous finding showed that the presence of RAS is associated with poor coronary collateral development and adverse 5-year outcome. Impaired arteriogenesis might partly explain the poor prognosis in RAS patients. This study aimed to investigate the impact of RAS on arteriogenesis and explore the possible role of interleukin-6 in this pathophysiological process.
METHODS: SHR rat was used as a control, while WKY rat underwent left renal artery coarctation to establish a two-kidney one-clip model with a 0.25mm silver clip at the left renal artery. Seven days after the left renal artery coarctation or sham operation, hind limb ischemia was induced by ligation of the left femoral artery. Blood pressure and heart rate were recorded every week. Laser Doppler perfusion imaging was performed at baseline, immediately after femoral ligation, at 14 and 28 days postfemoral artery ligation. Serum and hind limb tissue were collected for later analysis.
RESULTS: At the end of this study, no significant difference in blood pressure or heart rate was found between SHR and RAS rats. However, when treated with tocilizumab (TCZ), blood pressure was significantly lowered in RAS rats. Twenty-eight days after left femoral artery ligation, left hind limb perfusion was significantly worse in RAS rats than in SHR, and angiogenesis in the soleus muscle was similar between the groups, suggesting impaired arteriogenesis in RAS rats compared to SHR. Although the number of adductor muscle arterioles in RAS rats was not less than that of SHR, the mean inner diameter of arterioles in RAS rats was smaller than that of SHR. When treated with the TCZ, left hind limb perfusion in the RAS+TCZ rat was not improved. TCZ lowered serum and tissue levels of IL-6 in RAS+TCZ rats. Serum creatinine was mildly elevated in the RAS group.
DISCUSSION: Since blood pressure was similar between SHR and RAS rats, and TCZ failed to improve arteriogenesis in the RAS+TCZ group, we think that IL-6 might not be the primary mediator leading to impaired arteriogenesis in RAS rats. It seems that renal dysfunction induced by renal ischemia might have more chance to impair collateral development than hypertension or IL-6 in RAS rats.
CONCLUSION: Existence of RAS is associated with worse arteriogenesis, which might explain the increased risk of cardiovascular death and all-cause death in patients with RAS. IL-6 might not be responsible for impaired arteriogenesis in RAS rats. Possible mechanisms need to be investigated further.
METHODS: SHR rat was used as a control, while WKY rat underwent left renal artery coarctation to establish a two-kidney one-clip model with a 0.25mm silver clip at the left renal artery. Seven days after the left renal artery coarctation or sham operation, hind limb ischemia was induced by ligation of the left femoral artery. Blood pressure and heart rate were recorded every week. Laser Doppler perfusion imaging was performed at baseline, immediately after femoral ligation, at 14 and 28 days postfemoral artery ligation. Serum and hind limb tissue were collected for later analysis.
RESULTS: At the end of this study, no significant difference in blood pressure or heart rate was found between SHR and RAS rats. However, when treated with tocilizumab (TCZ), blood pressure was significantly lowered in RAS rats. Twenty-eight days after left femoral artery ligation, left hind limb perfusion was significantly worse in RAS rats than in SHR, and angiogenesis in the soleus muscle was similar between the groups, suggesting impaired arteriogenesis in RAS rats compared to SHR. Although the number of adductor muscle arterioles in RAS rats was not less than that of SHR, the mean inner diameter of arterioles in RAS rats was smaller than that of SHR. When treated with the TCZ, left hind limb perfusion in the RAS+TCZ rat was not improved. TCZ lowered serum and tissue levels of IL-6 in RAS+TCZ rats. Serum creatinine was mildly elevated in the RAS group.
DISCUSSION: Since blood pressure was similar between SHR and RAS rats, and TCZ failed to improve arteriogenesis in the RAS+TCZ group, we think that IL-6 might not be the primary mediator leading to impaired arteriogenesis in RAS rats. It seems that renal dysfunction induced by renal ischemia might have more chance to impair collateral development than hypertension or IL-6 in RAS rats.
CONCLUSION: Existence of RAS is associated with worse arteriogenesis, which might explain the increased risk of cardiovascular death and all-cause death in patients with RAS. IL-6 might not be responsible for impaired arteriogenesis in RAS rats. Possible mechanisms need to be investigated further.