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Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
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Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
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The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
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Coronary Artery Disease (CAD) is a primary health risk worldwide, leading to significant morbidity and mortality. The condition arises from the buildup of atherosclerotic plaques within the coronary arteries, resulting in diminished blood supply to the heart muscle.The clinical manifestations of CAD vary widely, from asymptomatic stages to severe, life-threatening conditions. Understanding these manifestations is crucial for early diagnosis and effective management.Angina Pectoris: The Warning...
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Pathological Circulating Factors in Moyamoya Disease.

Yao-Ching Fang1, Ling-Fei Wei1, Chaur-Jong Hu1,2

  • 1Taipei Neuroscience Institute, Taipei Medical University, Taipei 11031, Taiwan.

International Journal of Molecular Sciences
|February 11, 2021
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Summary

Moyamoya disease (MMD) involves narrowed brain vessels and abnormal collaterals. This study explores how circulating angiogenic factors contribute to MMD development and the formation of "Moyamoya vessels".

Keywords:
Moyamoya diseaseRNF213cerebrovascular diseasecirculating factorcollateral formationsgrowth factors

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Area of Science:

  • Neurology
  • Vascular Biology
  • Genetics

Background:

  • Moyamoya disease (MMD) is characterized by cerebrovascular stenosis and a network of collateral vessels.
  • The precise pathogenic mechanisms underlying MMD remain incompletely understood.
  • Genetic factors like RNF213 variations are implicated, but other factors are also suspected.

Purpose of the Study:

  • To summarize the hypothesized pathophysiology of Moyamoya disease.
  • To explore the role of circulating angiogenic factors in MMD pathogenesis.
  • To investigate the interactive modulation between these circulating factors.

Main Methods:

  • Literature review and synthesis of existing research on MMD.
  • Analysis of proposed mechanisms involving circulating angiogenic factors.
  • Hypothesizing the pathway from circulating factors to "Moyamoya vessels".

Main Results:

  • Circulating angiogenic factors, including growth factors, progenitor cells, and inflammatory mediators, are implicated in MMD.
  • These factors may promote intimal hyperplasia, endothelial hyperplasia, smooth muscle migration, and atypical neovascularization.
  • The study outlines a hypothesized pathway for how these factors contribute to the characteristic "Moyamoya vessels".

Conclusions:

  • Circulating angiogenic factors are likely critical in the development of Moyamoya disease.
  • Understanding these factors and their interactions may reveal new therapeutic targets for MMD.
  • Further research is needed to elucidate the exact mechanisms and validate the hypothesized pathways.