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Related Concept Videos

Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...

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Related Experiment Video

Updated: May 8, 2026

Characterization of Immune Cell-derived Extracellular Vesicles and Studying Functional Impact on Cell Environment
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Extracellular vesicles from post-COVID-19 patients alter endothelial function under protein restriction.

Geiza Rafaela Bobato1, Juliana Quinholi Rocha1, Daniele Mendes Guizoni1

  • 1Instituto de Biologia, Universidade Estadual de Campinas (UNICAMP), Campinas, Brazil.

American Journal of Physiology. Cell Physiology
|August 29, 2025
PubMed
Summary

Extracellular vesicles from severe COVID-19 survivors with malnutrition impair blood vessel function by increasing hydrogen peroxide. This finding highlights a potential mechanism for long-term cardiovascular issues post-COVID-19.

Keywords:
endothelial cellsendothelial functionextracellular vesiclespost-COVIDprotein restriction

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Author Spotlight: Advancing the Analysis of Plasma Extracellular Vesicle Proteome for Cardiovascular Biomarker Studies
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Area of Science:

  • Cardiovascular Biology
  • Infectious Disease Immunology
  • Nutritional Science

Background:

  • The COVID-19 pandemic exacerbated global food insecurity and malnutrition.
  • Protein restriction is linked to adverse COVID-19 outcomes and cardiovascular disease.
  • Post-COVID-19 syndrome involves endothelial dysfunction, potentially mediated by extracellular vesicles (EVs).

Purpose of the Study:

  • To investigate the role of extracellular vesicles (EVs) in endothelial cell (EC) dysfunction in long-term COVID-19, especially with protein malnutrition.
  • To determine if EVs from post-COVID-19 patients affect aortic endothelial function under malnourished conditions.

Main Methods:

  • Isolated circulating EVs from patients 1 and 6 months post-hospital discharge for severe COVID-19.
  • Assessed endothelial relaxation in mouse aortas after 3 months on normoprotein or low-protein diets (LP).
  • Evaluated EC death, nitric oxide (NO), and hydrogen peroxide (H2O2) levels in vitro under amino acid restriction.

Main Results:

  • Low-protein diet impaired endothelium-dependent relaxation, which was restored by post-COVID EVs.
  • This EV effect was dependent on catalase activity and linked to reduced catalase and increased 4-HNE adducts in LP mouse aortas.
  • In vitro, post-COVID EVs increased H2O2 in amino acid-restricted ECs, but not under normal conditions.

Conclusions:

  • EVs from patients 1-6 months after severe COVID-19 can impair aortic endothelial function.
  • This impairment is exacerbated by malnutrition and involves increased hydrogen peroxide (H2O2) contribution.
  • These findings suggest a mechanism linking post-COVID-19 endothelial dysfunction to malnutrition.