ArticleNature cardiovascular research2024
Klf9 is essential for cardiac mitochondrial homeostasis.
Article in Nature cardiovascular research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Single-Cell Mapping Identifies Aging-Associated Neutrophil Remodeling Across Multiple Organs.Aging cell · 2026Article
- 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
- Single-nucleus RNA sequencing reveals the pathological process and key transcription factor of sorafenib-induced cardiotoxicity.BMC medicine · 2026Article
- Nrf2 promotes NLRP3 inflammasome assembly and activation by Klf9-TXNIP axis.Cell death discovery · 2026Article
- Senescence modulated cardiac repair with pluripotent stem cell-derived cardiomyocytes.Stem cell research & therapy · 2026Article
- Beyond the Powerhouse: Mitochondrial Crosstalk as a Master Regulator of Cardiac Metabolic Homeostasis and Failure.Journal of cardiovascular translational research · 2026Review
- LVAD Therapy Improves Metabolic and Inflammatory State in the Heart.JACC. Basic to translational science · 2026Article
- Enalaprilat reverses neutrophil polarization imbalance via targeting taurine-STING axis for treatment of diabetic wounds.Cell reports. Medicine · 2026Article
- Endothelial Klf9 fine-tunes Akt signaling to act as a transcriptional brake restraining retinal angiogenesis.International journal of biological sciences · 2026Article
- Acupuncture alleviates secondary brain injury in intracerebral hemorrhage-induced rats through activating the LKLF/Mfn2 pathway.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026Article
- Mitochondrial remodeling in heart failure with reduced ejection fraction.Frontiers in physiology · 2026Review
- Constitutive expression of cardiomyocyte Klf9 precipitates metabolic dysfunction and spontaneous cardiomyopathy.Cellular signalling · 2025Article
- Insights into mitofusin-2 and endoplasmic reticulum stress regulation in adipose-derived mesenchymal stem cells senescence.World journal of stem cells · 2025Article
- KLF9-Mediated Transcriptional Promotion of HMGB2 Accelerates Cardiomyocyte Apoptosis, Inflammation, and Ferroptosis in Myocardial Ischemia/Reperfusion Injury.Cardiovascular toxicology · 2025Article
- Bavachin ameliorates cisplatin-induced nephrotoxicity by enhancing mitochondrial β-oxidation and lipid metabolism through MFN2.Molecular medicine (Cambridge, Mass.) · 2025Article
- Klf9 promotes the repair of myocardial infarction by regulating macrophage recruitment and polarization.JCI insight · 2025Article
- Histone H2A.Z Deacetylation and Dedifferentiation in Infarcted/Tip60-depleted Cardiomyocytes.bioRxiv : the preprint server for biology · 2025Article
- Variational autoencoder enhanced analysis of energy metabolism and autophagy in exercising cardiomyocytes.Experimental biology and medicine (Maywood, N.J.) · 2025Article
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dynamics and mitophagy are intimately linked physiological processes that are essential for cardiac homeostasis. Here we show that cardiac Krüppel-like factor 9 (Klf9) is dysregulated in human and rodent cardiomyopathy. Both global and cardiac-specific Klf9-deficient mice displayed hypertrophic cardiomyopathy. Klf9 knockout led to mitochondrial disarray and fragmentation, impairing mitochondrial respiratory function in cardiomyocytes. Furthermore, cardiac Klf9 deficiency inhibited mitophagy, thereby causing accumulation of dysfunctional mitochondria and acceleration of heart failure in response to angiotensin II treatment. In contrast, cardiac-specific Klf9 transgene improved cardiac systolic function. Mechanistically, Klf9 knockout decreased the expression of PGC-1α and its target genes involved in mitochondrial energy metabolism. Moreover, Klf9 controlled the expression of Mfn2, thereby regulating mitochondrial dynamics and mitophagy. Finally, adeno-associated virus-mediated Mfn2 rescue in Klf9-CKO hearts improved cardiac mitochondrial and systolic function. Thus, Klf9 integrates cardiac energy metabolism, mitochondrial dynamics and mitophagy. Modulating Klf9 activity may have therapeutic potential in the treatment of heart failure.
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Registered trials
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