Abstract:Low serum levels of caveolin-1 are an independent predictor of sHT after r-tPA administration. Because of the small sample size, further research is needed to validate these data.
“…sHT is an important clinical outcome of AIS patients, increasing the worse prognosis together with asHT (49). According to a recent study, about 8% of patients will develop sHT and subsequent worsening of the outcomes after thrombolysis therapies (50). However, due to the limited number FIGURE 4 | Multivariate adjusted odds ratios for the association between FIB-4 score and the subcategorized groups of HT (including HT, HI, and PH, respectively).…”
Background: Hemorrhagic transformation (HT) is a frequent, often asymptomatic event that occurs after acute ischemic stroke (AIS). Liver fibrosis, usually subclinical, is common and crucial in the development of liver disease. We aimed to investigate the association between liver fibrosis and HT in patients with AIS. Methods: We performed a single-center and retrospective study. A total of 185 consecutive participants with HT and 199 age-and sex-matched stroke patients without HT were enrolled in this study. We calculated one validated fibrosis index-Fibrosis-4 (FIB-4) score-to assess the extent of liver fibrosis. HT was detected by routine CT or MRI and was radiologically classified as hemorrhagic infarction type 1 or 2 or parenchymal hematoma type 1 or 2. HT was also classified into asymptomatic or symptomatic. We used logistic regression models adjusted for previously established risk factors to assess the risks for HT. Results: The median FIB-4 score was significantly higher among patients who developed HT than among those without HT, whereas standard hepatic assays were largely normal. Patients were assigned to groups of high FIB-4 score and low FIB-4 score based on the optimal cutoff value. Compared with the subjects in the low-FIB-4-score group, incidence of HT for the high-FIB-4-score group was significantly higher. After adjustment for potential confounders, the patients with high FIB-4 score had 3.461-fold risk of HT in AIS compared to the patients with low FIB-4 score [odds ratio, 3.461 (95% CI, 1.404-8.531)]. Conclusion: Liver fibrosis, measured by FIB-4 score, was independently associated with the risk of HT in AIS patients.
“…sHT is an important clinical outcome of AIS patients, increasing the worse prognosis together with asHT (49). According to a recent study, about 8% of patients will develop sHT and subsequent worsening of the outcomes after thrombolysis therapies (50). However, due to the limited number FIGURE 4 | Multivariate adjusted odds ratios for the association between FIB-4 score and the subcategorized groups of HT (including HT, HI, and PH, respectively).…”
Background: Hemorrhagic transformation (HT) is a frequent, often asymptomatic event that occurs after acute ischemic stroke (AIS). Liver fibrosis, usually subclinical, is common and crucial in the development of liver disease. We aimed to investigate the association between liver fibrosis and HT in patients with AIS. Methods: We performed a single-center and retrospective study. A total of 185 consecutive participants with HT and 199 age-and sex-matched stroke patients without HT were enrolled in this study. We calculated one validated fibrosis index-Fibrosis-4 (FIB-4) score-to assess the extent of liver fibrosis. HT was detected by routine CT or MRI and was radiologically classified as hemorrhagic infarction type 1 or 2 or parenchymal hematoma type 1 or 2. HT was also classified into asymptomatic or symptomatic. We used logistic regression models adjusted for previously established risk factors to assess the risks for HT. Results: The median FIB-4 score was significantly higher among patients who developed HT than among those without HT, whereas standard hepatic assays were largely normal. Patients were assigned to groups of high FIB-4 score and low FIB-4 score based on the optimal cutoff value. Compared with the subjects in the low-FIB-4-score group, incidence of HT for the high-FIB-4-score group was significantly higher. After adjustment for potential confounders, the patients with high FIB-4 score had 3.461-fold risk of HT in AIS compared to the patients with low FIB-4 score [odds ratio, 3.461 (95% CI, 1.404-8.531)]. Conclusion: Liver fibrosis, measured by FIB-4 score, was independently associated with the risk of HT in AIS patients.
“…In a clinical study, low serum levels of caveolin-1 were considered to be a predictor of symptomatic hemorrhagic transformation (sHT). sHT is related to increased endothelial permeability after r-tPA administration [71]. Fig.…”
Ischemic stroke starts a series of pathophysiological processes that cause brain injury. Caveolin-1 (cav-1) is an integrated protein and locates at the caveolar membrane. It has been demonstrated that cav-1 can protect blood–brain barrier (BBB) integrity by inhibiting matrix metalloproteases (MMPs) which degrade tight junction proteins. This article reviews recent developments in understanding the mechanisms underlying BBB dysfunction, neuroinflammation, and oxidative stress after ischemic stroke, and focuses on how cav-1 modulates a series of activities after ischemic stroke. In general, cav-1 reduces BBB permeability mainly by downregulating MMP9, reduces neuroinflammation through influencing cytokines and inflammatory cells, promotes nerve regeneration and angiogenesis via cav-1/VEGF pathway, reduces apoptosis, and reduces the damage mediated by oxidative stress. In addition, we also summarize some experimental results that are contrary to the above and explore possible reasons for these differences.
“…Results showed circulating Cav-1 levels in stroke patients were higher than those of healthy controls, while the basic level of serum Cav-1 in patients with substantive and symptomatic hemorrhage was lower than that in other patients. The level of serum Cav-1 in patients with hemorrhagic transformation remained stable within 72 h after stroke, while the level of serum Cav-1 in other patients decreased during this period, suggesting that a low serum Cav-1 level can be used as an independent predictor of hemorrhagic transformation after r-tPA treatment [40].…”
Section: Molecular Regulatory Mechanisms Of Caveolae-mediated Transcytosis In Is 41 Cav-1mentioning
Blood-brain barrier (BBB) disruption following ischemic stroke (IS) contributes to hemorrhagic transformation, brain edema, increased neural dysfunction, secondary injury, and mortality. Brain endothelial cells form a para and transcellular barrier to most blood-borne solutes via tight junctions (TJs) and rare transcytotic vesicles. The prevailing view attributes the destruction of TJs to the resulting BBB damage following IS. Recent studies define a stepwise impairment of the transcellular barrier followed by the paracellular barrier which accounts for the BBB leakage in IS. The increased endothelial transcytosis that has been proven to be caveolae-mediated, precedes and is independent of TJs disintegration. Thus, our understanding of post stroke BBB deficits needs to be revised. These recent findings could provide a conceptual basis for the development of alternative treatment strategies. Presently, our concept of how BBB endothelial transcytosis develops is incomplete, and treatment options remain limited. This review summarizes the cellular structure and biological classification of endothelial transcytosis at the BBB and reviews related molecular mechanisms. Meanwhile, relevant transcytosis-targeted therapeutic strategies for IS and research entry points are prospected.
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