Cellular and Molecular Mechanisms of Diabetic Atherosclerosis: Herbal Medicines as a Potential Therapeutic Approach

Tian, Jinfan; Liu, Yanfei; Liu, Yue; Chen, Ke-ji; Lyu, Shuzheng

doi:10.1155/2017/9080869

Cited by 23 publications

(10 citation statements)

References 129 publications

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“…AS is a primary instigator of coronary artery disease and manifests itself in other conditions including cerebrovascular disease as well as cardiovascular events such as myocardial infarctions, all of which are accompanied by high mortality and morbidity worldwide (Mach et al, 2008;Rader and Daugherty, 2008). Although several therapeutic approaches can be employed for the treatment of AS, there are subgroups of high risk patients who fail to benefit from existing treatment modalities (Ren et al, 2017;Tian et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

RETRACTED: PRDM16 Upregulation Induced by MicroRNA-448 Inhibition Alleviates Atherosclerosis via the TGF-β Signaling Pathway Inactivation

Liu¹,

Song²,

Ji³

et al. 2020

Front. Physiol.

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The dysregulated expression of microRNAs (miRs) has been associated with pathological and physiological processes of atherosclerosis (AS). In addition, PR domain-containing 16 (PRDM16), a transcriptional mediator of brown fat cell identity and smooth muscle cell activities, may be involved in the hypercholesterolemia during development of AS. The bioinformatic analysis identified a regulatory miR-448 of PRDM16. Hence, the current study aimed to explore whether miR-448 influenced the activities of aortic smooth muscle cell (ASMCs) in AS. We validated that miR-448 was highly expressed in peripheral blood of patients with AS and aortic smooth muscle of AS model mice. Whereas, PRDM16 was downregulated in the aortic smooth muscle of AS model mice. PRDM16 overexpression was observed to inhibit oxidative stress injury and cell proliferation, and promote apoptosis of ASMCs. Mechanistic studies revealed that miR-448 targeted PRDM16 and negatively regulated the PRDM16 expression, while PRDM16 blocked the TGF-β signaling pathway. Furthermore, Downregulated miR-448 alleviated oxidative stress injury, and attenuated ASMC cell proliferation, migration and enhanced cell apoptosis through upregulation of PRDM16. Taken together, silencing of miR-448 upregulates PRDM16 and inactivates the TGF-β signaling pathway, thereby impeding development of AS by repressing the proliferation, migration and invasion of ASMCs.

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Section: Introductionmentioning

confidence: 99%

RETRACTED: PRDM16 Upregulation Induced by MicroRNA-448 Inhibition Alleviates Atherosclerosis via the TGF-β Signaling Pathway Inactivation

Liu¹,

Song²,

Ji³

et al. 2020

Front. Physiol.

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“…The increased prevalence of diabetes mellitus is considered one of the greatest public health challenges nowadays. Type 1 diabetes mellitus (T1DM), a polygenic autoimmune disease, is resulted from both genetic and environmental factors [ 1 ]. Although T1DM has a lower prevalence compared with type 2 diabetes mellitus (T2DM), it is the most common form of diabetes in childhood and has a greater impact on the quality of living life.…”

Section: Introductionmentioning

confidence: 99%

Association of PD-1 and PD-L1 Genetic Polymorphyisms with Type 1 Diabetes Susceptibility

Qian

Guo

Chen

et al. 2018

Journal of Diabetes Research

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Aims The programmed death- (PD-) 1/PD-1 ligand (PD-L) pathway plays an important role in regulating T cell activation and maintaining peripheral tolerance. Accumulated studies showed that PD-1/PD-L1 pathway was involved in the development of type 1 diabetes (T1DM). Since the genetic background of type 1 diabetes differs greatly among the different population, we aim to investigate the association of genetic polymorphisms in PD-1 and PD-L1 with T1DM susceptibility in Chinese population. Methods In total, 166 T1DM patients and 100 healthy controls were enrolled into the study. Genomic DNA was extracted from 4 mL peripheral blood samples collected from each subject. Genotyping of 8 selected SNPs of PD-1 and PD-L1 was carried out by the pyrosequencing PSQ 24 System using PyroMark Gold reagents (QIAGEN). Results SNP rs4143815 in PD-L1 was significantly associated with T1DM. People carrying the C allele of rs4143815 suffering less risk of T1DM and T1DM patients with G/G genotype showed higher levels of autoantibody (AAB) positive incidence compared with C allele carriers. No significant associations were found in other SNPs. Conclusions Our results indicate that rs4143815 of PD-L1 is significantly associated with T1DM and may serve as a new biomarker to predict the T1DM susceptibility.

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“…Numerous clinical studies showed that patients with hyperglycemia are more prone to AS-related diseases [109], and blood glucose therapies effectively prevent cardiovascular diseases [110]. Hyperglycemia-linked endothelial dysfunction may correlate with increased vascular permeability, upregulation of adhesion molecules, chemokines, and ROS [111,112]. Hyperglycemia also contributed to the atherogenic modification of LDL and triggered the pathological accumulation of lipids in AS plaque [113].…”

Section: Hyperglycemiamentioning

confidence: 99%

Potential Role of Melatonin as an Adjuvant for Atherosclerotic Carotid Arterial Stenosis

Zhang

et al. 2021

Molecules

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Carotid artery stenosis (CAS) is an atherosclerotic disease characterized by a narrowing of the artery lumen and a high risk of ischemic stroke. Risk factors of atherosclerosis, including smoking, hypertension, hyperglycemia, hyperlipidemia, aging, and disrupted circadian rhythm, may potentiate atherosclerosis in the carotid artery and further reduce the arterial lumen. Ischemic stroke due to severe CAS and cerebral ischemic/reperfusion (I/R) injury after the revascularization of CAS also adversely affect clinical outcomes. Melatonin is a pluripotent agent with potent anti-inflammatory, anti-oxidative, and neuroprotective properties. Although there is a shortage of direct clinical evidence demonstrating the benefits of melatonin in CAS patients, previous studies have shown that melatonin may be beneficial for patients with CAS in terms of reducing endothelial damage, stabilizing arterial plaque, mitigating the harm from CAS-related ischemic stroke and cerebral I/R injury, and alleviating the adverse effects of the related risk factors. Additional pre-clinical and clinical are required to confirm this speculation.

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Cellular and Molecular Mechanisms of Diabetic Atherosclerosis: Herbal Medicines as a Potential Therapeutic Approach

Cited by 23 publications

References 129 publications

RETRACTED: PRDM16 Upregulation Induced by MicroRNA-448 Inhibition Alleviates Atherosclerosis via the TGF-β Signaling Pathway Inactivation

RETRACTED: PRDM16 Upregulation Induced by MicroRNA-448 Inhibition Alleviates Atherosclerosis via the TGF-β Signaling Pathway Inactivation

Association of PD-1 and PD-L1 Genetic Polymorphyisms with Type 1 Diabetes Susceptibility

Potential Role of Melatonin as an Adjuvant for Atherosclerotic Carotid Arterial Stenosis

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