ArticleEndocrine2018
Kaempferol attenuates hyperglycemia-induced cardiac injuries by inhibiting inflammatory responses and oxidative stress.
Article in Endocrine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
What it found
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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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Bibliometric and visual analysis of global publications on kaempferol.Frontiers in nutrition · 2024Pooled it
- Polyphenol-Mediated Modulation of Oxidative Stress Pathways in Type 1 Diabetes: A Systematic Review.Antioxidants (Basel, Switzerland) · 2026Review
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Polyphenols and Alzheimer's Disease: A Review on Molecular and Therapeutic Insights With In Silico Support.Food science & nutrition · 2025Review
- A comprehensive review on diabetic cardiomyopathy (DCM): histological spectrum, diagnosis, pathogenesis, and management with conventional treatments and natural compounds.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Exploring the Multi-Faceted Effects of Berberine in Ameliorating Diastolic Dysfunction in Rats with Heart Failure with Preserved Ejection Fraction.International journal of molecular sciences · 2025Article
- Sea buckthorn flavonoids and their derivatives: potential natural compounds for the treatment of diabetic cardiomyopathy.Frontiers in pharmacology · 2025Review
- The role of Nrf2 signaling pathway in diabetic cardiomyopathy: from pathogenesis to traditional Chinese medicine interventions.Frontiers in cardiovascular medicine · 2025Review
- Mechanism of Qilong Capsule against Myocardial Ischemia-Reperfusion Injury Based on Network Pharmacology and Experimental Validation.Combinatorial chemistry & high throughput screening · 2025Article
- [CompoundNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Characterization of Bioactive Metabolites and Antioxidant Activities in Solid and Liquid Fractions of Fresh Duckweed (ACS omega · 2024Article
- A Review on the Natural Products in Treatment of Diabetic Cardiomyopathy (DCM).Reviews in cardiovascular medicine · 2024Review
- Oxidative stress signaling in the pathogenesis of diabetic cardiomyopathy and the potential therapeutic role of antioxidant naringenin.Redox report : communications in free radical research · 2023Review
- Molecular targets and mechanisms ofWorld journal of diabetes · 2023Article
- A review of how the saffron (Crocus sativus) petal and its main constituents interact with the Nrf2 and NF-κB signaling pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Promising Therapeutic Treatments for Cardiac Fibrosis: Herbal Plants and Their Extracts.Cardiology and therapy · 2023Review
- Cardioprotective Properties of Kaempferol: A Review.Plants (Basel, Switzerland) · 2023Review
- Exploring the Complex Relationship between Diabetes and Cardiovascular Complications: Understanding Diabetic Cardiomyopathy and Promising Therapies.Biomedicines · 2023Review
- Costunolide alleviates hyperglycaemia-induced diabetic cardiomyopathy via inhibiting inflammatory responses and oxidative stress.Journal of cellular and molecular medicine · 2023Article
- Preliminary verification of the anti-hypoxia mechanism of Gentiana straminea maxim based on UPLC-triple TOF MS/MS and network pharmacology.BMC complementary medicine and therapies · 2022Article
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 at 2 institutions in 2 countries.
Funding
Abstract
purposeSuppression of inflammation and oxidative stress is an attractive strategy to against diabetic cardiomyopathy (DCM). Kaempferol (KPF) exerts both anti-inflammatory and antioxidant pharmacological properties. However, little is known about the effect of KPF on protecting myocardial injury in diabetes. The present study aimed to investigate the effect of KPF on DCM and underlying mechanism.
methodsAnti-inflammation and anti-oxidative stress activities of KPF were evaluated in H9c2 cells or primary cardiomyocytes by real-time quantitate PCR, immunoblotting, immunofluorescence, ELISA, and FACS. Streptozotocin (STZ)-induced type 1 diabetes mellitus mice were constructed. Corresponding to experiments in vitro, the therapeutic effect of KPF was also assessed using heart tissues from mice.
resultsKPF significantly inhibited high glocose (HG) induced expression of inflammatory cytokines and generation of ROS, leading to reduced fibrotic responses and cell apoptosis in vitro. KPF mediated DCM protective effects through inhibiting nuclear factor-κB (NF-κB) nucleus translocation and activating nuclear factor-erythroid 2 p45-related factor-2 (Nrf-2). In STZ-induced type 1 diabetic mouse model, KPF prevented diabetes-induced cardiac fibrosis and apoptosis. These changes were also accompanied by reducing inflammation and oxidative stress in diabetic mice hearts.
conclusionKPF is a potential therapeutic agent for the treatment of DCM, mechanically linked to inhibition of NF-κB and Nrf-2 activation.
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What 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.