ArticleCells2022
KLF9 Aggravates Streptozotocin-Induced Diabetic Cardiomyopathy by Inhibiting PPARγ/NRF2 Signalling.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 30 citations in OpenAlex.
- Dysregulation of the KLF9/TXNRD2 Axis Leads to Mitochondrial DNA Oxidation and NLRP3 Inflammasome Activation in Ulcerative Colitis.Journal of biochemical and molecular toxicology · 2026Article
- Analysis of Allele-Specific Expression Highlights Novel Participants of Empagliflozin-Driven Effects on T2DM-Associated Regulatory Pathways.International journal of molecular sciences · 2026Article
- KLF9 Aggravates Doxorubicin-Induced Cardiotoxicity by Regulating the ROS/p53 Signalling Pathway.Cardiovascular toxicology · 2026Article
- Endothelial microparticles in high glucose environment: molecular pathways of GDM-associated placental dysfunction and coenzyme Q10-based targeted therapy.Journal of nanobiotechnology · 2026Article
- Salvianolic acid A reduces lipotoxicity injury of cardiomyocytes by orchestrating oxidative stress and inflammation via Akt/Nrf2/NF-κB axis.Journal of molecular histology · 2025Article
- Constitutive expression of cardiomyocyte Klf9 precipitates metabolic dysfunction and spontaneous cardiomyopathy.Cellular signalling · 2025Article
- Resveratrol Alleviates Effects of LPS on Estrogen Synthesis, Oxidative Stress, Inflammation, and Pyroptosis of Goat Granulosa Cells by Activating the PPARG/NRF2/HO-1 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Screening Based on Structural and Biological Verification of Stachyose as a PPARγ-Modulating Ligand for the Treatment of Non-Alcoholic Fatty Liver Disease.Food science & nutrition · 2025Article
- Lipid Droplets Metabolism Mediated by ANXA7-PPARγ Signaling Axis Regulates Spinal Cord Injury Repair in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- KLF9, Epigenetic Silenced by DNMT1, Promotes ERK-Mediated Ferroptosis of Osteoarthritic Chondrocytes Through Transcriptionally Regulating CYP1B1.Journal of cellular and molecular medicine · 2025Article
- KLF9 aggravates the cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy through the lncRNA UCA1/p27 axis.International journal of experimental pathology · 2025Article
- Krüppel-like factors in mitochondrial quality control.Frontiers in physiology · 2025Review
- Echinacoside activates Nrf2/PPARγ signaling pathway to modulate mitochondrial fusion-fission balance to ameliorate ox-LDL-induced dysfunction of coronary artery endothelial cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- MARK4 aggravates cardiac dysfunction in mice with STZ-induced diabetic cardiomyopathy by regulating ACSL4-mediated myocardial lipid metabolism.Scientific reports · 2024Article
- Intermittent Fasting-Improved Glucose Homeostasis Is Not Entirely Dependent on Caloric Restriction in db/db Male Mice.Diabetes · 2024Article
- Natural Products and Health.Nutrients · 2024Article
- Krüpple-like factors in cardiomyopathy: emerging player and therapeutic opportunities.Frontiers in cardiovascular medicine · 2024Review
- Review
- Prdx6 Regulates Nlrp3 Inflammasome Activation-Driven Inflammatory Response in Lens Epithelial Cells.International journal of molecular sciences · 2023Article
- The Protective Effect of 11-Keto-β-Boswellic Acid against Diabetic Cardiomyopathy in Rats Entails Activation of AMPK.Nutrients · 2023Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsKrüppel-like Factor 9 (KLF9) is a transcription factor that regulates multiple disease processes. Studies have focused on the role of KLF9 in the redox system. In this study, we aimed to explore the effect of KLF9 on diabetic cardiomyopathy. METHODS AND
resultsCardiac-specific overexpression or silencing of KLF9 in C57BL/6 J mice was induced with an adeno-associated virus 9 (AAV9) delivery system. Mice were also subjected to streptozotocin injection to establish a diabetic cardiomyopathy model. In addition, neonatal rat cardiomyocytes were used to assess the possible role of KLF9 in vitro by incubation with KLF9 adenovirus or small interfering RNA against KLF9. To clarify the involvement of peroxisome proliferator-activated receptors (PPARγ), mice were subjected to GW9662 injection to inhibit PPARγ. KLF9 was upregulated in the hearts of mice with diabetic cardiomyopathy and in cardiomyocytes. In addition, KLF9 overexpression in the heart deteriorated cardiac function and aggravated hypertrophic fibrosis, the inflammatory response and oxidative stress in mice with diabetic cardiomyopathy. Conversely, cardiac-specific silencing of KLF9 ameliorated cardiac dysfunction and alleviated hypertrophy, fibrosis, the cardiac inflammatory response and oxidative stress. In vitro, KLF9 silencing in cardiomyocytes enhanced inflammatory cytokine release and oxidative stress; KLF9 overexpression increased these detrimental responses. Moreover, KLF9 was found to regulate the transcription of PPARγ, which suppressed the expression and nuclear translocation of nuclear Factor E2-related Factor 2 (NRF2). In mice injected with a PPARγ inhibitor, the protective effects of KLF9 knockdown on diabetic cardiomyopathy were counteracted by GW9662 injection.
conclusionsKLF9 aggravates cardiac dysfunction, the inflammatory response and oxidative stress in mice with diabetic cardiomyopathy. KLF9 may become a therapeutic target for diabetic cardiomyopathy.
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