AI Article Synopsis
- The JAK/STAT pathway's chronic activation is associated with oxidative stress, inflammation, and cell growth, and is regulated negatively by SOCS proteins, particularly SOCS1.
- Researchers studied PS5, a mimetic of the SOCS1's inhibitory region, for its potential as a treatment for conditions like diabetes and atherosclerosis through both lab tests and animal studies.
- Results showed that PS5 reduced inflammatory gene expression and atheroma plaque size while enhancing antioxidant genes, suggesting its promise as an effective antioxidant therapy for atherosclerosis.
Article Abstract
The chronic activation of the Janus kinase/signal transducer and activator of the transcription (JAK/STAT) pathway is linked to oxidative stress, inflammation and cell proliferation. Suppressors of cytokine signaling (SOCS) proteins negatively regulate the JAK/STAT, and SOCS1 possesses a small kinase inhibitory region (KIR) involved in the inhibition of JAK kinases. Several studies showed that KIR-SOCS1 mimetics can be considered valuable therapeutics in several disorders (e.g., diabetes, neurological disorders and atherosclerosis). Herein, we investigated the antioxidant and atheroprotective effects of PS5, a peptidomimetic of KIR-SOCS1, both in vitro (vascular smooth muscle cells and macrophages) and in vivo (atherosclerosis mouse model) by analyzing gene expression, intracellular O production and atheroma plaque progression and composition. PS5 was revealed to be able to attenuate NADPH oxidase (NOX1 and NOX4) and pro-inflammatory gene expression, to upregulate antioxidant genes and to reduce atheroma plaque size, lipid content and monocyte/macrophage accumulation. These findings confirm that KIR-SOCS1-based drugs could be excellent antioxidant agents to contrast atherosclerosis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7465353 | PMC |
| http://dx.doi.org/10.3390/antiox9080754 | DOI Listing |
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