ArticlePediatric research2026
HMGB1/MYH9 suppresses PPARγ to induce lung injury in renal ischemia-reperfusion: protective effects of Rosiglitazone.
Article in Pediatric research, 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe co-occurrence of acute kidney injury (AKI) and acute lung injury (ALI) is strongly associated with increased mortality. Understanding the role of high mobility group box 1 (HMGB1) in AKI-induced ALI is essential for identifying effective biomarkers and therapeutic targets.
methodsWe investigated the regulatory mechanism of HMGB1 and myosin heavy chain 9 (MYH9), as well as the effects of Rosiglitazone, a PPARγ agonist, in AKI-induced ALI using C57BL/6J mouse models of renal ischemia-reperfusion injury (IRI) and a renal-lung cell co-culture system.
resultsFollowing renal IRI, elevated serum HMGB1 interacted with lung MYH9, thereby inhibiting PPARγ-a key regulator of inflammation and endothelial barrier integrity-leading to increased levels of CCL2 and impaired endothelial barrier integrity, which ultimately resulted in ALI. Pretreatment with Rosiglitazone restored PPARγ function, reduced inflammation, and alleviated kidney and lung damage. Its therapeutic efficacy in mice was correlated with serum CCL2 levels. Furthermore, in a cohort of 421 critically ill children, higher urinary CCL2 levels were strongly associated with an increased risk of AKI/ALI and poorer survival outcomes.
conclusionThese findings underscore Rosiglitazone's therapeutic potential in AKI-induced ALI and highlight urinary CCL2 as a promising biomarker for treatment monitoring and outcome prediction in pediatric patients. IMPACT: HMGB1 released following renal ischemia-reperfusion binds MYH9 in lungs, suppressing PPARγ, driving inflammation and endothelial barrier dysfunction, thereby contributing to ALI pathogenesis. Rosiglitazone, a PPARγ agonist, restores PPARγ activity, strengthens barriers, reduces inflammation, and mitigates AKI-induced ALI in mouse models, with efficacy tied to serum CCL2 levels. Clinically, elevated urinary CCL2 in critically ill children associates with higher risk of concurrent AKI/ALI and poorer prognosis, indicating CCL2 as a biomarker for treatment response and prognosis. This work highlights a central pathogenic mechanism in AKI-ALI and proposes Rosiglitazone as a potential preventive/therapeutic strategy, with CCL2 guiding clinical monitoring.
Identifiers
42618600What OpenQuestion 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 OpenQuestion graph.