ArticleChinese journal of integrative medicine2026
Jinshui Huanxian Formula Combined with Exercise Rehabilitation Improves Skeletal Muscle Mitochondrial Damage in Treatment of Pulmonary Fibrosis by AMPK/mTOR/HIF-1 Pathway.
Article in Chinese journal of integrative medicine, 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
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo identify the effects and possible mechanism of Jinshui Huanxian Formula (JHF) combined with exercise rehabilitation (ER) in treatment of pulmonary fibrosis (PF).
methodsSixty male Sprague-Dawley rats were divided into 6 groups using a random number table, including control, model, pirfenidone [PFD, 54 mg/(kg•d)], ER, JHF [3.12 g/(kg•d)], and JHF combined with ER (JHF-ER) groups (n=10 per group). PF model was established by intratracheal instillation of bleomycin (5 mg/kg). Interventions were initiated on day 14 post-modeling and continued for 28 consecutive days. Pulmonary function, lung histopathology, and hydroxyproline (HYP) content were measured to evaluate anti-fibrotic effects. Hindlimb grip strength (HGS), exhaustive exercise time (ET), and skeletal muscle histopathology were assessed to determine skeletal muscle dysfunction improvement. The comprehensive R-value analysis was performed to compare the overall efficacy of different interventions. Mitochondrial function, transcriptomic profiling, and immunohistochemical staining were further conducted to elucidate the molecular mechanism of JHF-ER.
resultsInterventions with PFD, ER, JHF, and JHF-ER all ameliorated PF and skeletal muscle dysfunction to varying degrees (P<0.05 or P<0.01). Comprehensive R-value analysis revealed that JHF-ER exhibited superior overall therapeutic efficacy than PFD, ER and JHF mono-therapies (P<0.01). JHF-ER restored skeletal muscle mitochondrial function by inhibiting abnormal mitochondrial permeability transition pore opening and up-regulating adenosine triphosphate content and mitochondrial respiratory chain complexes I-IV activity (P<0.05 or P<0.01). Transcriptomic and experimental validation revealed that JHF-ER exerted these effects by inhibiting the AMP-activated protein kinase/mammalian target of rapamycin/hypoxia-inducible factor-1 (AMPK/mTOR/HIF-1) signaling pathway and suppressing excessive skeletal muscle mitophagy.
conclusionJHF-ER exhibited the potential to improve PF, enhance exercise tolerance, alleviate mitochondrial damage of skeletal muscle, which may be achieved by inhibiting the AMPK/mTOR/HIF-1 signaling pathway to inhibit mitophagy in skeletal muscle.
Indexed as
Identifiers
42995304What 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.