ArticleProceedings of the National Academy of Sciences of the United States of America2003
Cardiomyocyte-restricted knockout of STAT3 results in higher sensitivity to inflammation, cardiac fibrosis, and heart failure with advanced age.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 162 papers.
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Who cites it
162 citing papers in PubMed, 350 citations in OpenAlex.
- Article
- JAK1/2 inhibitor ruxolitinib reduces aggregates in cardiac proteinopathy.EMBO molecular medicine · 2026Article
- Causal relevance of the JAK/STAT pathway for cardioprotection via cold acclimation.Scientific reports · 2026Article
- Circulating Biomarkers in Elderly Patients with Heart Failure: A Real-Life Study.Antioxidants (Basel, Switzerland) · 2026Article
- Therapeutic potential of hookworm proteins in promoting regulatory immune responses to modulate Trypanosoma cruzi induced liver inflammation and oxidative stress.Memorias do Instituto Oswaldo Cruz · 2026Article
- STAT3 SH2 Domain Aspartic Acid 661 Mutations Activate Immune Gene Programs.Journal of cellular and molecular medicine · 2026Article
- The spectrum of pregnancy-induced cardiac remodeling: transitioning from healthy adaptive hypertrophy to peripartum cardiomyopathy.Frontiers in cell and developmental biology · 2026Review
- Cardiomyocyte Janus kinase 1 (JAK1) signaling is required for cardiac homeostasis and cytokine-dependent activation of STAT3.Journal of molecular and cellular cardiology · 2025Article
- Article
- Targeting the Gut-Heart Axis Improves Cardiac Remodeling in a Clinical Scale Model of Cardiometabolic Syndrome.JACC. Basic to translational science · 2025Article
- The anti-aging potential of antihypertensive peptides ofFrontiers in aging · 2025Article
- Sex and Age Differences in the Impact of Metabolic Syndrome on Heart Failure Development.Metabolites · 2024Review
- The Role of FNDC4 in Inflammation and Metabolism for Various Diseases.Aging and disease · 2024Review
- MiR-4763-3p accelerates lipopolysaccharide-induced cardiomyocyte apoptosis and inflammatory response by targeting IL10RA.Cytotechnology · 2024Article
- STAT protein family and cardiovascular diseases: overview of pathological mechanisms and therapeutic implications.Molecular biology reports · 2024Review
- scaRNA20 promotes pseudouridylatory modification of small nuclear snRNA U12 and improves cardiomyogenesis.Experimental cell research · 2024Article
- Molecular and Cellular Mechanisms Underlying the Cardiac Hypertrophic and Pro-Remodelling Effects of Leptin.International journal of molecular sciences · 2024Review
- The MEF2A transcription factor interactome in cardiomyocytes.Cell death & disease · 2023Article
- Activating α7nAChR helps post-myocardial infarction healing by regulating macrophage polarization via the STAT3 signaling pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Cadherin-11-Interleukin-6 Signaling between Cardiac Fibroblast and Cardiomyocyte Promotes Ventricular Remodeling in a Mouse Pressure Overload-Induced Heart Failure Model.International journal of molecular sciences · 2023Article
102 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Cytokines and inflammation have been implicated in the pathogenesis of heart failure. For example, IL-6 family cytokines and the gp130 receptor play important roles in cardiac myocyte survival and hypertrophy. Signal transducer and activator of transcription 3 (STAT3) is a major signaling protein that is activated through gp130. We have created mice with a cardiomyocyte-restricted deletion of STAT3. As measured by serial echocardiograms, mice with cardiac specific deletion of STAT3 are significantly more susceptible to cardiac injury after doxorubicin treatment than age-matched controls. Intriguingly, STAT3 appears to have a critical role in protection of inflammation-induced heart damage. STAT3-deficient mice treated with lipopolysaccharide demonstrated significantly more apoptosis than their WT counterparts. At the cellular level, cardiomyocytes with STAT3 deleted secrete significantly more tumor necrosis factor in response to lipopolysaccharide than those with WT STAT3. Furthermore, histologic examination of the cardiomyocyte-restricted STAT3-deficient mice reveals a dramatic increase in cardiac fibrosis in aged mice. Although no overt signs of heart failure are present in young STAT3-deficient mice, they spontaneously develop heart dysfunction with advancing age. These results indicate the crucial functions of STAT3 in cardiomyocyte resistance to inflammation and other acute injury and in pathogenesis of age-related heart failure.
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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.