Publications by authors named "Ranzun Zhao"

Despite significant advancements in drug-eluting stent technology, in-stent restenosis (ISR) still occurs in approximately 10 % of patients undergoing percutaneous coronary intervention, remaining a significant global health concern. The mechanisms underlying ISR are complex and multifactorial, yet recent innovations in intravascular imaging and functional assessment have substantially advanced our understanding, enabling more targeted and personalized therapies. This review synthesizes the latest insights into ISR, emphasizing the pivotal roles of advanced imaging modalities, such as optical coherence tomography (OCT) and intravascular ultrasound, and functional assessments like quantitative flow ratio and optical flow ratio in guiding ISR management.

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The aim of this study was to explore the relationship between in-stent neoatherosclerosis (ISNA) and the neutrophil-to-lymphocyte ratio (NLR) in patients with in-stent restenosis (ISR) following drug-eluting stent (DES) implantation. We divided 216 patients into 3 groups based on the NLR tertile. We performed a comparative analysis of baseline, angiographic, and features of optical coherence tomography (OCT) between the NLR groups and performed univariate and multivariate logistic regression analyses to assess the association of the NLR with ISNA and in-stent thin-cap fibroatheroma (TCFA).

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Article Synopsis
  • The study investigates how N6-methyladenosine (m6A) regulation, particularly the protein YTHDC1, can improve the survival of bone marrow mesenchymal stem cells (BMSCs) used in treating myocardial infarction (MI).
  • Researchers found that YTHDC1 levels were decreased under conditions that induce cell death, and enhancing its expression in BMSCs decreased cell death and reactive oxygen species (ROS) production.
  • In rat models of MI, BMSCs with overexpressed YTHDC1 led to better heart function and reduced tissue damage, highlighting YTHDC1's potential as a target for improving BMSC therapies in heart damage.
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Background: Cholesterol crystals (CCs) are recognized as a risk factor for vulnerable atherosclerotic plaque rupture (PR) and major adverse cardiovascular events. However, their predictive factors and association with plaque vulnerability in patients with acute myocardial infarction (AMI) remain insufficiently explored. Therefore, This study aims to investigate the association between CCs and plaque vulnerability in culprit lesions of AMI patients, identify the factors influencing CCs formation, and develop a predictive model for CCs.

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Objective: Patients with infectious intracranial aneurysms (IIAs) have high mortality rates. Sepsis is an important condition that induces IIA. Smooth muscle cell (SMC) phenotypic switching may have a critical effect on sepsis-induced IIA, but its role remains unclear.

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Background: In-stent neoatherosclerosis (ISNA) is identified as the primary cause of in-stent restenosis (ISR). The systemic immune inflammation index (SII), shows promise for predicting post-percutaneous coronary intervention (PCI) adverse cardiovascular events and is associated with coronary stenosis severity; however, its specific relationship with ISNA remains unclear. This study aimed to investigate the association between the SII and ISNA after drug-eluting stent (DES) implantation.

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Rationale: Tachycardia is a common arrhythmia in clinical practice, and its pathogenesis is mostly related to reentry. However, there are also a few tachycardia that are not related to reentry. Actively clarifying the pathogenesis of these non-reentry related tachycardia is of great significance for its treatment.

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Background: Stent malapposition (SM) following percutaneous coronary intervention (PCI) for myocardial infarction continues to present significant clinical challenges. In recent years, machine learning (ML) models have demonstrated potential in disease risk stratification and predictive modeling.

Hypothesis: ML models based on optical coherence tomography (OCT) imaging, laboratory tests, and clinical characteristics can predict the occurrence of SM.

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Background: Neoatherosclerosis (NA) is associated with stent failure. However, systematic studies on the manifestations of NA and neovascularization (NV) at different stages after drug-eluting stent (DES) implantation are lacking. Moreover, the relationship between NA and NV in in-stent restenosis (ISR) has not been reported.

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Background: Hypoxia-induced pulmonary artery hypertension (HPH) is a complication of chronic hypoxic lung disease and the third most common type of pulmonary artery hypertension (PAH). Epigenetic mechanisms play essential roles in the pathogenesis of HPH. N6-methyladenosine (m6A) is an important modified RNA nucleotide involved in a variety of biological processes and an important regulator of epigenetic processes.

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Acute coronary syndrome (ACS), a significant cardiovascular disease threat, has garnered increased focus concerning its etiological mechanisms. Thin-cap fibroatheroma (TCFA) are central to ACS pathogenesis, characterized by lipid-rich plaques, profuse foam cells, cholesterol crystals, and fragile fibrous caps predisposed to rupture. While TCFAs may be latent and asymptomatic, their pivotal role in ACS risk is undeniable.

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Background: The relationship between neointimal characteristics of in-stent restenosis (ISR) and periprocedural myocardial injury (PMI) remains unclear. Therefore, this study aimed to investigate the relationship between PMI and neointimal characteristics of ISR by using optical coherence tomography (OCT).

Methods: This was a retrospective study.

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Neoatherosclerosis is a major cause of stent failure after percutaneous coronary intervention. Metabolism such as hyperuricemia is associated with in-stent restenosis (ISR). However, the association between serum uric acid (sUA) levels and in-stent neoatherosclerosis (ISNA) has never been validated.

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Hypoxia, characterized by reduced oxygen concentration, is a significant stressor that affects the survival of aerobic species and plays a prominent role in cardiovascular diseases. From the research history and milestone events related to hypoxia in cardiovascular development and diseases, The "hypoxia-inducible factors (HIFs) switch" can be observed from both temporal and spatial perspectives, encompassing the occurrence and progression of hypoxia (gradual decline in oxygen concentration), the acute and chronic manifestations of hypoxia, and the geographical characteristics of hypoxia (natural selection at high altitudes). Furthermore, hypoxia signaling pathways are associated with natural rhythms, such as diurnal and hibernation processes.

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Cardiac macrophages with different polarization phenotypes regulate ventricular remodeling and neovascularization after myocardial infarction (MI). Annexin A2 (ANXA2) promotes macrophage polarization to the repair phenotype and regulates neovascularization. However, whether ANXA2 plays any role in post-MI remodeling and its underlying mechanism remains obscure.

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Neoatherosclerosis (NA) is a significant contributor to late stent failure; however, predictors of late in-stent restenosis (ISR) with NA have not been systematically reported. This study aimed to identify predictors of NA incidence and plaque vulnerability in patients with late ISR and the role of low-density lipoprotein cholesterol (LDL-C) levels in this process. A total of 216 patients with 216 lesions who underwent optical coherence tomography (OCT) before interventional procedure for late drug-eluting stent ISR were enrolled and divided into NA and non-NA groups based on OCT findings.

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Background: Monocyte-to-high-density lipoprotein cholesterol ratio (MHR) is an independent predictor of atherosclerosis and in-stent restenosis (ISR). However, the association between MHR and the incidence of in-stent neoatherosclerosis (ISNA) remains to be validated.

Methods: This study included 216 patients with acute coronary syndrome who had 220 ISR lesions and had undergone optical coherence tomography (OCT).

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M2 macrophage-mediated tissue repair plays an important role in acute myocardial infarction (AMI). Additionally, VSIG4, which is mainly expressed on tissue-resident and M2 macrophages, is crucial for the regulation of immune homeostasis; however, its effects on AMI remain unknown. In this study, we aimed to investigate the functional significance of VSIG4 in AMI using knockout and adoptive bone marrow transfer chimeric models.

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N6-methylatidine (m6A) is involved in post-transcriptional metabolism and a variety of pathological processes. However, little is known about the role of m6A in vascular proliferative diseases, particularly in vascular smooth muscle cells (VSMCs) phenotype switching-induced neointimal hyperplasia. In the current study, we discovered that methyltransferase like 3 (METTL3) is a critical candidate for catalyzing a global increase in m6A in response to carotid artery injury and various VSMCs phenotype switching.

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We aimed to explore the effects of myeloid-derived growth factor (Mydgf) on the regulation of hypoxia/reoxygenation (HR)-induced apoptosis of cardiac microvascular endothelial cells (CMECs). CMECs were exposed to hypoxia for 24 h and reoxygenation for 6 h to establish an HR cell model. Subsequently, an adenovirus was used to overexpress Mydgf in CMECs.

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Myocardial infarction is one of the leading diseases causing death and disability worldwide, and the revascularization of damaged tissues is essential for myocardial-injury repair. Circular RNAs (circRNAs) are widely involved in physiological and pathological processes in various systems throughout the body, and the role of circRNAs in cardiovascular disease is gaining attention. In this study, we determined that circERBB2IP is highly expressed in the hearts of newborn mice.

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Article Synopsis
  • Exosomes from cardiomyocytes (CMs) may influence angiogenesis by delivering microRNA (miR) specifically miR-29a, which has a role in regulating both angiogenesis and myocardial hypertrophy.
  • The study utilized Angiotensin II (Ang II) to induce hypertrophy in CMs and examined the effects of exosomes on cardiac microvascular endothelial cells (CMECs) in various assays, highlighting the role of miR-29a.
  • Findings indicated that Ang II-induced CMs release exosomal miR-29a, which inhibits the proliferation and angiogenic functions of CMECs by targeting and suppressing the expression of vascular endothelial growth factor A (VEGFA).
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Background: The in-hospital mortality of patients with ST-segment elevation myocardial infarction (STEMI) increases to more than 50% following a cardiogenic shock (CS) event. This study highlights the need to consider the risk of delayed calculation in developing in-hospital CS risk models. This report compared the performances of multiple machine learning models and established a late-CS risk nomogram for STEMI patients.

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Accurate risk assessment of high-risk patients is essential in clinical practice. However, there is no practical method to predict or monitor the prognosis of patients with ST-segment elevation myocardial infarction (STEMI) complicated by hyperuricemia. We aimed to evaluate the performance of different machine learning models for the prediction of 1-year mortality in STEMI patients with hyperuricemia.

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