Decoding the PI3K/Akt/mTOR-JAK/STAT signaling axis in multiple sclerosis: mechanistic crosstalk and therapeutic opportunities.
What this study shows
Review mapping the mechanistic crosstalk between PI3K/Akt/mTOR and JAK/STAT pathways in MS neuroinflammation, identifying dual-pathway mTOR targeting as a therapeutic opportunity to reduce immune dysregulation and demyelination.
At a glance
| Evidence type | R Review — secondary literature, not a new result Marked R because it is a review or synthesis of existing evidence rather than a new primary result; that is a different form of writing, not a weaker one. |
| Study type | Narrative Review |
| Model system | Review |
| Journal | Immunologic research |
| Year | 2026 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1007/s12026-026-09808-9 · PMID 42467315 |
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | mTOR inhibitors (proposed therapeutic) |
| Target | PI3K/Akt/mTOR-JAK/STAT axis |
| Model | N/A (review) |
| Effect | PI3K/Akt/mTOR-JAK/STAT crosstalk drives neuroinflammation in MS; mTOR inhibition proposed as treatment |
In the Atlas
Related topics
More studies on this topic
- The phosphoinositide 3-kinase pathway (2002)
- IGF2BP3-Mediated m6A Modification of OLR1 mRNA Promotes Immune Evasion in CRC via the PI3K/AKT/mTOR Pathway (2026)
- A dynamic network model of mTOR signaling reveals TSC-independent mTORC2 regulation (2012)
- A systems study reveals concurrent activation of AMPK and mTOR by amino acids (2016)
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