ArticleExperimental and therapeutic medicine2022
PTP1B inhibition ameliorates inflammatory injury and dysfunction in ox-LDL-induced HUVECs by activating the AMPK/SIRT1 signaling pathway via negative regulation of KLF2.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 19 citations in OpenAlex.
- Inhibition of PTP1B Through NADH Dehydrogenase Activity Reduces Acute Pancreatic Acinar Cell Pyroptosis by Inhibiting the ROS/TXNIP/NLRP3 Pathway.Digestive diseases and sciences · 2026Article
- Omentin-1 protects against endothelial dysfunction through the AMPK/KLF2/eNOS pathway in adult rat offspring exposed to maternal diabetes.Nutrition & diabetes · 2025Article
- From Tyrosine Kinases to Tyrosine Phosphatases: New Therapeutic Targets in Cancers and Beyond.Pharmaceutics · 2024Review
- New Dawn for Atherosclerosis: Vascular Endothelial Cell Senescence and Death.International journal of molecular sciences · 2023Review
- Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases.Journal of inflammation research · 2023Review
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Atherosclerosis is a key pathogenic factor of cardiovascular diseases. However, the role of protein tyrosine phosphatase 1B (PTP1B) in oxidized low-density lipoprotein (ox-LDL)-treated vascular endothelial cells remains unclear. The aim of the present study was to explore the possible physiological roles and mechanism of PTP1B in atherosclerosis using HUVECs as an
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.