Back to search

Article

Homocysteine Metabolites Inhibit Autophagy by Upregulating the Expression of miR-21-5p (LC3, p62, BECN1), miR-155-5p (ATG5, LC3), miR-216-5p (BECN1, ATG5, LC3) and miR-320c-3p (ATG7) in Human Vascular Endothelial Cells

2023-08-14

Abstract excerpt

Nutritional and genetic deficiencies in homocysteine (Hcy) metabolism lead to hyperhomocysteinemia (HHcy) and cause endothelial dysfunction, a hallmark of atherosclerosis, which is a major cause of cardiovascular disease (CVD). Impaired autophagy causes the accumulation of damaged proteins and organelles and is associated with CVD. Biochemically, HHcy is characterized by elevated levels of Hcy and its metabolites,...

Topics

Open a Topic to create a Post that cites this publication.

Identifiers and source

Literature Corpus work
971d7889-2f7e-57bc-b23d-61d19b4e5ee7
DOI
10.21203/rs.3.rs-3200508/v1
Open publication

Related research

Semantic proximity does not establish scientific evidence.

Click a neighbor to travelStep 1 · 12 closest
Interactive article relationship graphSelect a related publication card to move it into the centre and load its closest explainable connections. Solid lines are source-backed structured connections. Dashed lines are semantic discovery signals and are not scientific evidence.
Homocysteine Metabolites Inhibit Autophagy by Upregulating the Expression of miR-21-5p (LC3, p62, BECN1), miR-155-5p (ATG5, LC3), miR-216-5p (BECN1, ATG5, LC3) and miR-320c-3p (ATG7) in Human Vascular Endothelial CellsDOI 10.21203/rs.3.rs-3200508/v1
Select a neighboring publication to make it the new centre.