ArticleNature medicine2015
Tumor necrosis factor-α confers cardioprotection through ectopic expression of keratins K8 and K18.
Article in Nature medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 106 citations in OpenAlex.
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- Biomarkers of Cardiovascular Stress: A Historical Review.Journal of cardiovascular development and disease · 2026Review
- A journey through the molecular networks of endomyocardial biopsies to explore ATTR and ALiScience · 2026Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.Advanced healthcare materials · 2026Article
- Hypoxia conditioned adipose-derived stem cell-derived extracellular vesicle therapy improves cardiac function in a rat model of ischemic cardiomyopathy.Regenerative therapy · 2026Article
- Cell-type specific allelic dampening of sex-linked genes in sex chromosome aneuploidy.bioRxiv : the preprint server for biology · 2026Article
- Infusible Extracellular Matrix Biomaterial Enhances Cell-Specific Pro-Repair Responses Following Acute Myocardial Infarction.bioRxiv : the preprint server for biology · 2025Article
- Molecular insights into the role of desmin intermediate filament network in chromatin landscape, cardiomyocyte differentiation, and maturation.Cell death & disease · 2025Article
- A Comprehensive Review: Unraveling the Role of Inflammation in the Etiology of Heart Failure.Heart failure reviews · 2025Review
- Perinatal Exposure to Lead or Diethylhexyl Phthalate in Mice: Sex-Specific Effects on Cardiac DNA Methylation and Gene Expression across Time.Environmental health perspectives · 2025Article
- Whole tissue proteomic analyses of cardiac ATTR and AL unveil mechanisms of tissue damage.Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis · 2025Article
- Article
- A proteomic atlas of kidney amyloidosis provides insights into disease pathogenesis.Kidney international · 2024Article
- Systematic characterization of regulatory variants of blood pressure genes.Cell genomics · 2023Article
- Topologically associating domain underlies tissue specific expression of long intergenic non-coding RNAs.iScience · 2023Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Altered acylcarnitine metabolism and inflexible mitochondrial fuel utilization characterize the loss of neonatal myocardial regeneration capacity.Experimental & molecular medicine · 2023Article
- Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 8 institutions in 4 countries.
Funding
Abstract
Tumor necrosis factor-α (TNF-α), one of the major stress-induced proinflammatory cytokines, is upregulated in the heart after tissue injury, and its sustained expression can contribute to the development of heart failure. Whether TNF-α also exerts cytoprotective effects in heart failure is not known. Here we provide evidence for a cardioprotective function of TNF-α in a genetic heart failure model, desmin-deficient mice. The cardioprotective effects of TNF-α are a consequence of nuclear factor-κB (NF-κB)-mediated ectopic expression in cardiomyocytes of keratin 8 (K8) and keratin 18 (K18), two epithelial-specific intermediate filament proteins. In cardiomyocytes, K8 and K18 (K8/K18) formed an alternative cytoskeletal network that localized mainly at intercalated discs (IDs) and conferred cardioprotection by maintaining normal ID structure and mitochondrial integrity and function. Ectopic induction of K8/K18 expression in cardiomyocytes also occurred in other genetic and experimental models of heart failure. Loss of the K8/K18 network resulted in a maladaptive cardiac phenotype following transverse aortic constriction. In human failing myocardium, where TNF-α expression is upregulated, K8/K18 were also ectopically expressed and localized primarily at IDs, which did not contain detectable amounts of desmin. Thus, TNF-α- and NF-κB-mediated formation of an alternative, stress-induced intermediate filament cytoskeleton has cardioprotective function in mice and potentially in humans.
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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.