Publications by authors named "Xiangwen Xi"

Cardiovascular disease (CVD) is a major cause of unnatural death worldwide, so timely diagnosis of CVD is crucial for improving patient outcomes. Although the traditional diagnostic tools can locate plaque and observe inner wall of blood vessel structure, they commonly have radioactivity and cannot detect the chemical composition of the plaque accurately. Recently emerging Raman techniques can detect the plaque composition precisely, and have the advantages of being fast, high-resolution and marker-free.

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Article Synopsis
  • Klf9, a protein linked to heart health, is found to be dysregulated in heart disease, leading to issues like hypertrophic cardiomyopathy in mice.
  • Deleting Klf9 results in poorly functioning mitochondria and reduced mitophagy, which worsens heart failure when exposed to angiotensin II.
  • Enhancing Klf9 activity or rescuing related proteins can improve heart function, suggesting that targeting Klf9 may be a promising treatment for heart failure.
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  • The study investigates coronary artery calcification (CAC) as a significant indicator of atherosclerosis and its link to clinical outcomes, highlighting the need for better imaging analysis methods.* -
  • Researchers developed a deep learning technique to automatically identify and measure CAC using a large dataset of over 1 million OCT images from 1,048 patients, achieving nearly human-level accuracy in their assessments.* -
  • Analysis of 1,259 patients with ST-segment elevated myocardial infarctions showed that those with more severe calcification in the affected arteries faced a higher risk of major cardiovascular and cerebrovascular events, while calcification in other arteries was not significantly linked to these risks.*
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Background: Coronary artery calcification (CAC), a surrogate of atherosclerosis, is related to stent underexpansion and adverse cardiac events. However, the effect of CAC on plaque stability is still controversial and the morphological significance of CAC has yet to be elucidated.

Methods: A retrospective series of 419 patients with acute coronary syndrome (ACS) who underwent optical coherence tomography (OCT) were enrolled.

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  • Current atherosclerosis treatments struggle to reverse advanced plaque buildup, with high amino acid levels from a Western diet causing mTORC1-autophagy defects in macrophages, worsening the condition.* -
  • Research identified that the upregulation of Gpr137b-ps in atherosclerotic plaques impacts autophagy, with experiments on mice showing that reducing Gpr137b-ps enhances macrophage autophagy and reduces plaque lesions.* -
  • Gpr137b-ps seems to inhibit the binding of HSC70 to G3BP, which in turn affects mTORC1 signaling, suggesting targeting this pathway could offer a new avenue for treating advanced atherosclerosis.*
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Background: Cholesterol crystals (CCs) are regular microstructures found within the necrotic core of atherosclerotic plaques and have been hypothesized to be related to plaque destabilization. We attempted to investigate the potential association between CCs and non-culprit plaque vulnerability in patients with ST-segment elevated myocardial infarction (STEMI) and study morphological features of CCs in ruptured non-culprit plaques.

Methods: A total of 261 patients with ST-segment elevation myocardial infarction who underwent 3-vessel optical coherence tomography (OCT) imaging were included.

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Background: Cardiovascular disease is a leading cause of death, which signifies the urgent need for effective anti-atherosclerotic strategies. Gut microbiota-dependent trimethylamine-N-oxide (TMAO) is associated with atherosclerosis, and geraniin, a natural polyphenol with various biological activities, might play key role in this process.

Purpose: We aimed to investigate the pharmacological activity of geraniin in atherosclerosis through remodeling the gut microbiota.

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Acute coronary syndrome (ACS) is a group of clinical syndromes characterized by rupture or erosion of atherosclerotic unstable plaques. Effective intervention for vulnerable plaques (VP) is of great significance to reduce adverse cardiovascular events. Fbn1 mice were crossbred with LDLR mice to obtain a novel model for atherosclerotic VP.

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To identify differential mRNA and ncRNA expression profiles and competing endogenous RNA-associated regulatory networks during the progression of atherosclerosis (AS). We systematically analyzed whole-transcriptome sequencing of samples from different stages of AS to evaluate their long noncoding RNA (lncRNA), circular RNA (circRNA), miRNA and mRNA profiles. We constructed three AS-related competing endogenous RNA regulatory networks of differentially expressed circRNAs, lncRNAs, miRNAs and mRNAs.

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The coronavirus disease 19 (COVID-19) pandemic poses a serious global threat to human health and the economy. Based on accumulating evidence, its continuous progression involves not only pulmonary injury but also damage to the cardiovascular system due to intertwined pathophysiological risks. As a point of convergence in the pathophysiologic process between COVID-19 and heart failure (HF), cytokine storm induces the progression of COVID-19 in patients presenting pre-existing or new onset myocardial damage and even HF.

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Atherosclerosis is mediated by various factors and plays an important pathological foundation for cardiovascular and cerebrovascular diseases. Abnormal vascular smooth muscle cells (VSMCs) proliferation and migration have an essential role in atherosclerotic lesion formation. Circular RNAs (circRNA) have been widely detected in different species and are closely related to various diseases.

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Objective: Despite the current antiatherosclerotic and antithrombotic therapies, the incidence of advanced atherosclerosis-associated clinical events remains high. Whether long noncoding RNAs (lncRNAs) affect the progression of atherosclerosis and whether they are potential targets for the treatment of advanced atherosclerosis are poorly understood. Approach and Results: The progression of atherosclerotic lesions was accompanied by dynamic alterations in lncRNA expression, as revealed by RNA sequencing and quantitative polymerase chain reaction.

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Aims: This study aimed to investigate the progression and vascular shrinkage of vulnerable plaque lesions with a plaque burden at least 70% among patients with coronary artery disease by optical coherence tomography (OCT) and intravascular ultrasound (IVUS).

Methods: Fifty-six OCT-identified vulnerable plaques from 47 patients were included among coronary angiography-identified nonculprit/nontarget lesions. Serial IVUS images were used to assess plaque progression and vascular shrinkage.

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