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Sestrin2 Suppression Promotes Endothelial-Mesenchymal Transition and Exacerbates Methylglyoxal-Induc...

Sestrin2 Suppression Promotes Endothelial-Mesenchymal Transition and Exacerbates Methylglyoxal-Induc...

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_proquest_miscellaneous_3160920706

Sestrin2 Suppression Promotes Endothelial-Mesenchymal Transition and Exacerbates Methylglyoxal-Induced Endothelial Dysfunction

About this item

Full title

Sestrin2 Suppression Promotes Endothelial-Mesenchymal Transition and Exacerbates Methylglyoxal-Induced Endothelial Dysfunction

Publisher

Switzerland: MDPI AG

Journal title

International journal of molecular sciences, 2024-12, Vol.25 (24), p.13463

Language

English

Formats

Publication information

Publisher

Switzerland: MDPI AG

More information

Scope and Contents

Contents

Sestrin2 (SESN2) is a stress-inducible protein known for its cytoprotective functions, but its role in diabetic vascular complications remains unclear. This study investigated the impact of SESN2 on methylglyoxal (MGO)-induced endothelial-mesenchymal transition (EndMT). Human endothelial cells were transfected with SESN2 siRNA duplexes to silence S...

Alternative Titles

Full title

Sestrin2 Suppression Promotes Endothelial-Mesenchymal Transition and Exacerbates Methylglyoxal-Induced Endothelial Dysfunction

Identifiers

Primary Identifiers

Record Identifier

TN_cdi_proquest_miscellaneous_3160920706

Permalink

https://devfeature-collection.sl.nsw.gov.au/record/TN_cdi_proquest_miscellaneous_3160920706

Other Identifiers

ISSN

1422-0067,1661-6596

E-ISSN

1422-0067

DOI

10.3390/ijms252413463

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