ArticlePharmaceutical biology2021
Huoxue Qianyang Qutan recipe attenuates cardiac fibrosis by inhibiting the NLRP3 inflammasome signalling pathway in obese hypertensive rats.
Article in Pharmaceutical biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Who cites it
6 citing papers in PubMed.
- Huoxue Qianyang Qutan Recipe limits cardiac remodeling by regulating FUNDC1/IP3R2 signaling pathway in obese hypertensive rats.Scientific reports · 2026Article
- Obesity-Associated Cardiac Fibrosis: Mechanisms and Emerging Therapeutic Targets.Vascular health and risk management · 2026Review
- NLRP3 Inflammasome: A New Target for the Treatment of CVD and Depression Comorbidity.Mediators of inflammation · 2025Review
- Effects of NLRP3 Inflammasome Mediated Pyroptosis on Cardiovascular Diseases and Intervention Mechanism of Chinese Medicine.Chinese journal of integrative medicine · 2024Review
- The NLRP3 Inflammasome as a Novel Therapeutic Target for Cardiac Fibrosis.Journal of inflammation research · 2022Review
- Hypertension and its management in COVID-19 patients: The assorted view.International journal of cardiology. Cardiovascular risk and prevention · 2021Review
Corrections and comments
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
contextHuoXue QianYang QuTan Recipe (HQQR) is used to manage hypertension and cardiac remodelling, but the mechanism is elusive.
objectiveTo determine the mechanism of HQQR on obesity hypertension (OBH)-related myocardial fibrosis. MATERIALS AND
methodsOBH models were prepared using spontaneously hypertensive rats (SHRs) and divided (
resultsHQQR(H) reduced SBP (201.67 ± 21.00
conclusionHQQR blunted cardiac fibrosis development in OBH and suppressed CFs proliferation by directly interfering with the NLRP3/caspase-1/IL-1β pathway.
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Registered trials
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