ArticleJournal of diabetes investigation2026
Linderalactone mitigates diabetic renal injury by inhibiting macrophage inflammation via the Dectin1/Syk/CARD9/IRF5/NF-κB pathway.
Article in Journal of diabetes investigation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundInflammation plays an essential role in the pathogenesis of diabetic nephropathy (DN). Linderalactone (LNL), as a natural sesquiterpene lactone, has been discovered to have anti-inflammatory activation. However, the effects of linderalactone on diabetes-associated renal damage remain unclear.
methodsThis study investigated the effects of LNL on renal function and inflammation in diabetic mice. Renal function, collagen deposition, and fibrosis were assessed. RNA-sequencing was performed to identify molecular pathways affected by LNL. The Dectin1-related pathway was analyzed in kidney tissues and RAW264.7 cells. Dectin1-deficient and Dectin1-overexpressing models were used to confirm the mechanism of LNL.
resultsLNL improved renal function, reduced collagen deposition and fibrosis in diabetic mice without affecting blood glucose levels. RNA-sequencing revealed that LNL primarily impacted the Dectin1 pathway. It inhibited the Dectin1/Syk/CARD9/IRF5/NF-κB pathway, reduced macrophage and neutrophil infiltration, and suppressed inflammatory cytokine expression. Dectin1 knockdown mimicked these effects, while Dectin1 overexpression reversed them.
conclusionsLNL alleviates DN via suppression of macrophage inflammation by mediating the Dectin1/Syk/CARD9/IRF5/NF-κB signaling pathway, highlighting its potential as a therapeutic agent for diabetes-associated renal injury.
Indexed as
Identifiers
What Socratic holds
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.