Background: COVID-19 is a new coronavirus that constitutes a great challenge to human health. At this stage, there are still cases of COVID-19 infection in some countries and regions, in which ischemic stroke (IS) is a risk factor for new coronavirus pneumonia, and patients with COVID-19 infection have a dramatically elevated risk of stroke. At the same time, patients with long-term IS are vulnerable to COVID-19 infection and have more severe disease, and carotid atherosclerosis is an early lesion in IS.
Methods: This study used human induced pluripotent stem cell (hiPSC)-derived monolayer brain cell dataset and human carotid atherosclerosis genome-wide dataset to analyze COVID-19 infection and carotid atherosclerosis patients to determine the synergistic effect of new coronavirus infection on carotid atherosclerosis patients, to clarify the common genes of both, and to identify common pathways and potential drugs for carotid atherosclerosis in patients with COVID-19 infection RESULTS: Using several advanced bioinformatics tools, we present the causes of COVID-19 infection leading to increased mortality in carotid atherosclerosis patients and the susceptibility of carotid atherosclerosis patients to COVID-19. Potential therapeutic agents for COVID-19 -infected patients with carotid atherosclerosis are also proposed.
Conclusions: With COVID-19 being a relatively new disease, associations have been proposed for its connections with several ailments and conditions, including IS and carotid atherosclerosis. More patient-based data-sets and studies are needed to fully explore and understand the relationship.
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http://dx.doi.org/10.1016/j.jiph.2022.03.004 | DOI Listing |
As a key inflammatory factor, the nucleotide-binding oligomerization domain (NOD)-like receptor protein 3 (NLRP3) inflammasome plays a crucial role in neuroinflammation and the progression of neurodegenerative diseases. Dysregulation of NLRP3 signaling can trigger various inflammatory responses in the brain, contributing to the development of neurodegenerative diseases such as ischemic stroke, vascular dementia (VaD), Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS). Therefore, the NLRP3 signaling pathway is a promising therapeutic target for the treatment of neurodegenerative diseases, including VaD.
View Article and Find Full Text PDFThe Circle of Willis (CW) is a critical cerebrovascular structure that supports collateral blood flow to maintain brain perfusion and compensate for eventual occlusions. Increased tortuosity of highrisk vessels within the CW has been implicated as a marker in the progression of cerebrovascular diseases especially in structures like the internal carotid artery (ICA). This is partly due to age-related plaque deposition or arterial stiffening.
View Article and Find Full Text PDFClin Appl Thromb Hemost
January 2025
Department of Neurology, Liaocheng People's Hospital, Liaocheng, Shandong, China.
Background: Carotid artery stenosis (CAS) may cause many cerebrovascular diseases, and a biomarker for screening and monitoring is needed. This study focused on the clinical significance of long-chain non-coding RNA (lncRNA) non-coding RNA activated by DNA damage (NORAD) in patients with CAS and aimed to search for potential biomarkers of CAS.
Methods: Eighty-six asymptomatic patients with CAS and 60 healthy individuals were enrolled, with corresponding clinical data and serum samples collected.
Am J Case Rep
January 2025
Department of Otolaryngology, Sanford Medical Center Fargo, Fargo, ND, USA.
BACKGROUND Carotid artery injury has an incidence of 0.2% in the National Trauma Data Bank. The true incidence of intracranial carotid injury is unknown but can be estimated at less than one in 1000 trauma-related inpatient admissions in America.
View Article and Find Full Text PDFHepatol Int
January 2025
Division of Gastroenterology and Hepatology, Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan.
Background/purpose: Although metabolic dysfunction-associated steatotic liver disease (MASLD) has been proposed to replace the diagnosis of non-alcoholic fatty liver disease (NAFLD) with new diagnostic criteria since 2023, the genetic predisposition of MASLD remains to be explored.
Methods: Participants with data of genome-wide association studies (GWAS) in the Taiwan Biobank database were collected. Patients with missing data, positive for HBsAg, anti-HCV, and alcohol drinking history were excluded.
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