Carotid artery perivascular adipose tissue (PVAT) can influence plaque formation and progression. Recently, carotid artery PVAT density has emerged as a novel imaging biomarker being capable of reflecting local metabolic and inflammatory states of adipose tissue. It is closely associated with vulnerable plaque characteristics, such as intraplaque hemorrhage, thinning or rupture of the fibrous cap, lipid-rich necrotic core, and calcification. Therefore, carotid artery PVAT density holds promise as a key parameter for early identification of vulnerable carotid plaques and stroke risk prediction. This article reviews the definition and pathophysiological mechanism of PVAT and application of imaging techniques in PVAT, as well as the association between carotid artery PVAT density and vulnerable characteristics of plaques, with the aim of providing references for early identification of asymptomatic high-risk plaques and individualized prevention strategies of ischemic stroke.

Carotid artery perivascular adipose tissue (PVAT) can influence plaque formation and progression. Recently, carotid artery PVAT density has emerged as a novel imaging biomarker being capable of reflecting local metabolic and inflammatory states of adipose tissue. It is closely associated with vulnerable plaque characteristics, such as intraplaque hemorrhage, thinning or rupture of the fibrous cap, lipid-rich necrotic core, and calcification. Therefore, carotid artery PVAT density holds promise as a key parameter for early identification of vulnerable carotid plaques and stroke risk prediction. This article reviews the definition and pathophysiological mechanism of PVAT and application of imaging techniques in PVAT, as well as the association between carotid artery PVAT density and vulnerable characteristics of plaques, with the aim of providing references for early identification of asymptomatic high-risk plaques and individualized prevention strategies of ischemic stroke.

Objective To investigate the mechanism of mitochondrial division regulating myocardi-al fatty acid oxidation in diabetic mice.Methods A total of 16 7-week-old male SPF C57BLKS/J diabetic mice were randomly divided into model group and mitochondrial division inhibitor 1(mdivi-1)intervention group(intervention group),with 8 mice in each group.Another 8 male SPF C57BLKS/J mice of the same age were fed adaptively for 1 week and served as control group.The changes in blood glucose and body mass were monitored in above groups.Echocardiography was conducted to detect LVEF and LVFS1 rate and E/A between early and late ventricular diastole.The pathological changes of myocardial tissue were observed by HE staining.The size,morpholo-gy and quantity of mitochondria were observed by TEM.Western blotting was used to detect the expression of mitochondrial dynamin-related protein 1(Drp1),peroxisome proliferator activated receptor α(PPARα),long chain acyl-CoA synthetase 4(ACSL4),carnitine palmitoyl transferase 1B(CPT1B),and fatty acid oxidation detection kit was conducted to determine the activity of fat-ty acid oxidation.Results Compared with the control group,the model group presented hyper-trophic cardiomyocytes and significantly larger cross-sectional diameter of cardiomyocytes(22.36±2.80 μm vs 12.71±1.78 μm,P＜0.01)than the control group.Mdivi-1 intervention resul-ted in greatly improved myocardial hypertrophy and obviously smaller cross-sectional diameter of cardiomyocytes(13.79±1.39 μm vs 22.36±2.8 μm,P＜0.01)when compared with the model group.The expression level of myocardial mitochondrial Drp1,number of mitochondria per unit area of myocardial tissue and the protein levels of PPARα,ACSL4 and CPT1B in myocardial cyto-plasm were significantly higher,and the average mitochondrial area of myocardial tissue,the ex-pression of PPARα,ACSL4 and CPT1B in myocardial mitochondria,and fatty acid oxidation activ-ity were significantly lower in the model group than the control group(P＜0.01).After mdivi-1 intervention,the expression level of myocardial mitochondrial Drp1,the number of mitochondria per unit area of myocardial tissue and the protein levels of PPARα,ACSL4 and CPT1B in myocar-dial mitochondria were notably lower,and the expression of PPARα,ACSL4 and CPT1B in myo-cardial mitochondria and fatty acid oxidation activity in myocardial tissue were significantly higher when compared with those in the model group(P＜0.05,P＜0.01).Conclusion In diabetic mice,increased myocardial mitochondrial division,decreased translocation of fatty acid oxidation regula-tory protein from cytoplasm to mitochondria,inhibited fatty acid oxidation,and myocardial injury are observed.Mdivi-1 intervention inhibits mitochondrial division,promotes fatty acid oxidation by increasing the translocation of fatty acid oxidation regulatory proteins to mitochondria,and thus improves cardiac function.

The pathogenesis of diabetic cardiomyopathy(DCM)is the imbalance of glucose and lipid metabolism related to diabetes mellitus,that leads to increased oxidative stress and activation of various inflammatory pathways,causing cellular and extracellular damage,pathological cardiac remodeling,and diastolic and systolic dysfunction.Anti fibrotic drugs,anti-inflammatory drugs,and antioxidants are used in clinical treatment of DCM with good therapeutic effects.This article reviews the research progress on the pathogenesis and treatment strategies of DCM.

Objective To investigate the mechanism of mitochondrial division regulating myocardi-al fatty acid oxidation in diabetic mice.Methods A total of 16 7-week-old male SPF C57BLKS/J diabetic mice were randomly divided into model group and mitochondrial division inhibitor 1(mdivi-1)intervention group(intervention group),with 8 mice in each group.Another 8 male SPF C57BLKS/J mice of the same age were fed adaptively for 1 week and served as control group.The changes in blood glucose and body mass were monitored in above groups.Echocardiography was conducted to detect LVEF and LVFS1 rate and E/A between early and late ventricular diastole.The pathological changes of myocardial tissue were observed by HE staining.The size,morpholo-gy and quantity of mitochondria were observed by TEM.Western blotting was used to detect the expression of mitochondrial dynamin-related protein 1(Drp1),peroxisome proliferator activated receptor α(PPARα),long chain acyl-CoA synthetase 4(ACSL4),carnitine palmitoyl transferase 1B(CPT1B),and fatty acid oxidation detection kit was conducted to determine the activity of fat-ty acid oxidation.Results Compared with the control group,the model group presented hyper-trophic cardiomyocytes and significantly larger cross-sectional diameter of cardiomyocytes(22.36±2.80 μm vs 12.71±1.78 μm,P＜0.01)than the control group.Mdivi-1 intervention resul-ted in greatly improved myocardial hypertrophy and obviously smaller cross-sectional diameter of cardiomyocytes(13.79±1.39 μm vs 22.36±2.8 μm,P＜0.01)when compared with the model group.The expression level of myocardial mitochondrial Drp1,number of mitochondria per unit area of myocardial tissue and the protein levels of PPARα,ACSL4 and CPT1B in myocardial cyto-plasm were significantly higher,and the average mitochondrial area of myocardial tissue,the ex-pression of PPARα,ACSL4 and CPT1B in myocardial mitochondria,and fatty acid oxidation activ-ity were significantly lower in the model group than the control group(P＜0.01).After mdivi-1 intervention,the expression level of myocardial mitochondrial Drp1,the number of mitochondria per unit area of myocardial tissue and the protein levels of PPARα,ACSL4 and CPT1B in myocar-dial mitochondria were notably lower,and the expression of PPARα,ACSL4 and CPT1B in myo-cardial mitochondria and fatty acid oxidation activity in myocardial tissue were significantly higher when compared with those in the model group(P＜0.05,P＜0.01).Conclusion In diabetic mice,increased myocardial mitochondrial division,decreased translocation of fatty acid oxidation regula-tory protein from cytoplasm to mitochondria,inhibited fatty acid oxidation,and myocardial injury are observed.Mdivi-1 intervention inhibits mitochondrial division,promotes fatty acid oxidation by increasing the translocation of fatty acid oxidation regulatory proteins to mitochondria,and thus improves cardiac function.