ArticleDiabetology & metabolic syndrome2025
Honokiol attenuates diabetic nephropathy by targeting SIRT3 to suppress mitochondrial ROS-induced pyroptosis.
Article in Diabetology & metabolic syndrome, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Mitochondrial Regulation of the NLRP3 Inflammasome in Diabetic Kidney Disease: From Mechanisms to Therapeutic Strategies.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
backgroundDiabetic nephropathy (DN) persists as the leading cause of end-stage renal disease worldwide. Growing evidence indicates that mitochondrial dysfunction triggers NLRP3 inflammasome activation and subsequent pyroptosis, which play crucial roles in DN development. Honokiol (HKL), a natural compound with the ability to upregulate SIRT3 expression, shows promise in protecting mitochondrial function. This study investigates HKL's renoprotective effects in DN and explores its mechanism of action through the SIRT3-mediated regulation of mitochondrial ROS, NLRP3 inflammasome, and pyroptosis. MATERIALS AND
methodsdb/db diabetic mice and HK-2 cells subjected to hyperglycemic stimulation were used to assess the therapeutic effects of HKL. Renal function, pyroptosis, and mitochondrial homeostasis were assessed via biochemical assays, histopathological and immunohistochemical analyses, transmission electron microscopy, Western blotting, and immunofluorescence staining. SIRT3 overexpression and knockdown were performed to validate its regulatory role, while the mtROS scavenger MitoTEMPO was utilized to confirm the pivotal involvement of mtROS in the pyroptotic pathway.
resultsHKL treatment significantly ameliorated renal dysfunction and pathological damage in diabetic mice. Mechanistically, HKL upregulated SIRT3 expression, thereby improving mitochondrial function (maintaining structural integrity, stabilizing the membrane potential, and reducing mtROS accumulation), which in turn suppressed NLRP3 inflammasome activation and subsequent GSDMD-mediated pyroptosis. SIRT3 overexpression mimicked the protective effects of HKL, whereas SIRT3 knockdown attenuated its efficacy, confirming the essential role of SIRT3 in this process. Furthermore, mtROS scavenging by MitoTEMPO mitigated pyroptosis, reinforcing the dependence of the effects of HKL on the SIRT3-mtROS axis.
conclusionBy upregulating SIRT3 expression to maintain mitochondrial homeostasis and suppress mtROS-NLRP3-mediated pyroptosis, HKL emerges as a promising therapeutic strategy for DN.
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.