Publications by authors named "Erdan Dong"

Background: Kinesin family member 13B (KIF13B), a crucial motor protein, exerts multiple cellular biological functions. However, the implication of KIF13B in metabolic dysfunction-associated fatty liver disease (MAFLD) has not been explored yet. This study aimed to investigate KIF13B's role and underlying mechanism in MAFLD and proposes it as a potential pharmacological target.

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As a highly complex organ with digestive, endocrine, and immune-regulatory functions, the liver is pivotal in maintaining physiological homeostasis through its roles in metabolism, detoxification, and immune response. Various factors including viruses, alcohol, metabolites, toxins, and other pathogenic agents can compromise liver function, leading to acute or chronic injury that may progress to end-stage liver diseases. While sharing common features, liver diseases exhibit distinct pathophysiological, clinical, and therapeutic profiles.

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Diffuse-type tenosynovial giant cell tumor (dTGCT) is a destructive but rare benign proliferative synovial neoplasm. Although surgery is currently the main treatment modality for dTGCT, the recurrence risk is up to 50%. Therefore, there is a great need for effective drugs against dTGCT with minor side effects.

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Heart failure is characterized by abnormal β-adrenergic receptor (β-AR) activation and mitochondrial dysfunction. In heart failure, overactivation of β-AR mediates key pathological processes in cardiomyocytes, including oxidative stress, calcium overload and metabolic abnormalities, which subsequently lead to inflammation, myocardial apoptosis and necrosis. Mitochondria are the core organelles for energy metabolism, and also play a vital role in calcium homeostasis, redox balance and signaling transduction.

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  • Truncating mutations are significant contributors to cardiomyopathy, with different types of mutations presenting distinct cardiac issues in mouse models.
  • Germline mutations lead to defects in cardiac maturation, while cardiomyocyte-specific mutations cause pathological hypertrophy, but genetic mosaic mutations show no observable defects.
  • Treatment with adeno-associated virus (AAV) vectors to restore lamin-A demonstrated that targeting non-cardiomyocyte cells is crucial for improving cardiac health associated with these mutations.
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  • The study analyzed global statistics on liver diseases like alcohol-related liver disease (ALD), hepatitis B/C, liver cancer, and metabolic dysfunction-associated steatotic liver disease (MASLD), revealing trends in incidence, mortality, and disability-adjusted life years (DALYs) from 2000 to 2019.
  • While rates for ALD, MASLD, and other liver diseases increased, those for HBV, HCV, and liver cancer declined, with lower mortality in countries with a high socio-demographic index (SDI).
  • Research funding for MASLD and hepatobiliary cancer surged, but overall drug approvals for liver diseases remained low, particularly highlighting the lack of approved treatments for ALD.
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  • Cardiac ischemia/reperfusion (I/R) injury is a significant concern for heart disease, but there's currently no effective treatment to minimize this type of heart damage.
  • This study recruited patients with acute myocardial infarction to examine the impact of plasma RIPK3 levels before and after treatment, using both patient data and lab experiments on cells and mouse models.
  • Elevated RIPK3 levels post-treatment were linked to worse outcomes, and experiments showed that RIPK3 worsens heart injury by triggering inflammation, suggesting its role as a damaging molecule that could be targeted for therapy.
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  • Cardiac rehabilitation improves life quality and reduces illness in patients with coronary heart disease through exercise, lifestyle changes, and medical management.
  • Traditional methods assess endothelial function, but there's limited research on newer rehabilitation programs' effects on it.
  • Key benefits of exercise and lifestyle changes include enhanced nitric oxide availability, increased endothelial progenitor cells, and reduced oxidative stress, highlighting the need for comprehensive clinical trials to explore new protective strategies.
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Background And Purpose: Elevated levels of 5-HT have been correlated with coronary artery disease and cardiac events, suggesting 5-HT is a potential novel factor in the development of atherosclerotic cardiovascular disease. However, the underlying pathological mechanisms of the 5-HT system in atherosclerosis remain unclear. The 5-HT receptor (5-HT2BR), which establishes a positive feedback loop with 5-HT, has been identified as a contributor to pathophysiological processes in various vascular disorders.

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Background: β-adrenergic receptor (β-AR) overactivation is a major pathological cue associated with cardiac injury and diseases. AMPK (AMP-activated protein kinase), a conserved energy sensor, regulates energy metabolism and is cardioprotective. However, whether AMPK exerts cardioprotective effects via regulating the signaling pathway downstream of β-AR remains unclear.

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Background: Currently, pathophysiological mechanisms of post-acute sequelae of coronavirus disease-19-cardiovascular syndrome (PASC-CVS) remain unknown.

Methods And Results: Patients with PASC-CVS exhibited significantly higher circulating levels of severe acute respiratory syndrome-coronavirus-2 spike protein S1 than the non-PASC-CVS patients and healthy controls. Moreover, individuals with high plasma spike protein S1 concentrations exhibited elevated heart rates and normalized low frequency, suggesting cardiac β-adrenergic receptor (β-AR) hyperactivity.

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Z-discs are core ultrastructural organizers of cardiomyocytes that modulate many facets of cardiac pathogenesis. Yet a comprehensive proteomic atlas of Z-disc-associated components remain incomplete. Here, we established an adeno-associated virus (AAV)-delivered, cardiomyocyte-specific, proximity-labeling approach to characterize the Z-disc proteome in vivo.

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Unlabelled: Z-lines are core ultrastructural organizers of cardiomyocytes that modulate many facets of cardiac pathogenesis. Yet a comprehensive proteomic atlas of Z-line-associated components remain incomplete. Here, we established an adeno-associated virus (AAV)-delivered, cardiomyocyte-specific, proximity-labeling approach to characterize the Z-line proteome in vivo.

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Nanoparticles are promising tools for biomedicine. Many nanoparticles are internalized to function. Clathrin-mediated endocytosis is one of the most important mechanisms for nanoparticle internalization.

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Myocardial infarction and revascularization cause cardiac ischemia/reperfusion (I/R) injury featuring cardiomyocyte death and inflammation. The Ca/calmodulin dependent protein kinase II (CaMKII) family are serine/ threonine protein kinases that are involved in I/R injury. CaMKII exists in four different isoforms, α, β, γ, and δ.

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Blood-brain barrier (BBB) function deteriorates during aging, contributing to cognitive impairment and neurodegeneration. It is unclear what drives BBB leakage in aging and how it can be prevented. Using single-nucleus transcriptomics, we identified decreased connexin 43 (CX43) expression in cadherin-5 (Cdh5) cerebral vascular cells in naturally aging mice and confirmed it in human brain samples.

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Toll-like receptors (TLRs) are a family of pattern recognition receptors (PRRs) that can identify pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). TLRs play an important role in the innate immune response, leading to acute and chronic inflammation. Cardiac hypertrophy, an important cardiac remodeling phenotype during cardiovascular disease, contributes to the development of heart failure.

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Sympathetic stress is prevalent in cardiovascular diseases. Sympathetic overactivation under strong acute stresses triggers acute cardiovascular events including myocardial infarction (MI), sudden cardiac death, and stress cardiomyopathy. α-ARs and β-ARs, two dominant subtypes of adrenergic receptors in the heart, play a significant role in the physiological and pathologic regulation of these processes.

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Rapid over-activation of β-adrenergic receptors (β-AR) following acute stress initiates cardiac inflammation and injury by activating interleukin-18 (IL-18), however, the process of inflammation cascades has not been fully illustrated. The present study aimed to determine the mechanisms of cardiac inflammatory amplification following acute sympathetic activation. With bioinformatics analysis, galectin-3 was identified as a potential key downstream effector of β-AR and IL-18 activation.

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