ArticleCardiovascular research2014
Toll-interacting protein (Tollip) negatively regulates pressure overload-induced ventricular hypertrophy in mice.
Article in Cardiovascular research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Associations between genetic variants of Toll-interacting proteins and interstitial lung diseases: a systematic review and meta-analysis.Orphanet journal of rare diseases · 2024Pooled it
- Srxn1 Overexpression Protect Against Cardiac Remodelling by Inhibiting Oxidative Stress and Inflammation.Journal of cellular and molecular medicine · 2025Article
- From mitochondria to heart: the role and challenges of mitochondrial antiviral signaling protein in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
- Regulation of Key Immune-Related Genes in the Heart Following Burn Injury.Journal of personalized medicine · 2022Article
- MCC950 ameliorates ventricular arrhythmia vulnerability induced by heart failure.Bioengineered · 2022Article
- Tollip promotes hepatocellular carcinoma progression via PI3K/AKT pathway.Open medicine (Warsaw, Poland) · 2022Article
- The Akt pathway mediates the protective effects of myeloid differentiation protein 1 in pathological cardiac remodelling.ESC heart failure · 2021Article
- Toll-interacting protein impacts on inflammation, autophagy, and vacuole trafficking in human disease.Journal of molecular medicine (Berlin, Germany) · 2021Review
- MD1 deletion exaggerates cardiomyocyte autophagy induced by heart failure with preserved ejection fraction through ROS/MAPK signalling pathway.Journal of cellular and molecular medicine · 2020Article
- Article
- Schisandrin B attenuates pressure overload-induced cardiac remodeling in mice by inhibiting the MAPK signaling pathway.Experimental and therapeutic medicine · 2019Article
- TRAF1 Exacerbates Myocardial Ischemia Reperfusion Injury via ASK1-JNK/p38 Signaling.Journal of the American Heart Association · 2019Article
- MicroRNA-145 Protects against Myocardial Ischemia Reperfusion Injury via CaMKII-Mediated Antiapoptotic and Anti-Inflammatory Pathways.Oxidative medicine and cellular longevity · 2019Article
- Tollip Negatively Regulates Vascular Smooth Muscle Cell-Mediated Neointima Formation by Suppressing Akt-Dependent Signaling.Journal of the American Heart Association · 2018Article
- Loss of MD1 exacerbates pressure overload-induced left ventricular structural and electrical remodelling.Scientific reports · 2017Article
- Diet-induced obesity impairs spermatogenesis: a potential role for autophagy.Scientific reports · 2017Article
- Curcumin ameliorates high‑fat diet‑induced spermatogenesis dysfunction.Molecular medicine reports · 2016Article
- Regulator of G protein signalling 14 attenuates cardiac remodelling through the MEK-ERK1/2 signalling pathway.Basic research in cardiology · 2016Article
- The ubiquitin E3 ligase TRAF6 exacerbates pathological cardiac hypertrophy via TAK1-dependent signalling.Nature communications · 2016Article
- Characterization and expression analysis of Toll-interacting protein in common carp, Cyprinus carpio L., responding to bacterial and viral challenge.SpringerPlus · 2016Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
aimsToll-interacting protein (Tollip) is a critical regulator of the Toll-like receptor-mediated signalling pathway. However, the role of Tollip in chronic pressure overload-induced cardiac hypertrophy remains unclear. This study aimed to determine the functional significance of Tollip in the regulation of aortic banding-induced cardiac remodelling and its underlying mechanisms. METHODS AND
resultsFirst, we observed that Tollip was down-regulated in human failing hearts and murine hypertrophic hearts, as determined by western blotting and RT-PCR. Using cultured neonatal rat cardiomyocytes, we found that adenovirus vector-mediated overexpression of Tollip limited angiotensin II-induced cell hypertrophy; whereas knockdown of Tollip by shRNA exhibited the opposite effects. We then generated a transgenic (TG) mouse model with cardiac specific-overexpression of Tollip and subjected them to aortic banding (AB) for 8 weeks. When compared with AB-treated wild-type mouse hearts, Tollip-TGs showed a significant attenuation of cardiac hypertrophy, fibrosis, and dysfunction, as measured by echocardiography, immune-staining, and molecular/biochemical analysis. Conversely, a global Tollip-knockout mouse model revealed an aggravated cardiac hypertrophy and accelerated maladaptation to chronic pressure overloading. Mechanistically, we discovered that Tollip interacted with AKT and suppressed its downstream signalling pathway. Pre-activation of AKT in cardiomyocytes largely offset the Tollip-elicited anti-hypertrophic effects.
conclusionOur results provide the first evidence that Tollip serves as a negative regulator of pathological cardiac hypertrophy by blocking the AKT signalling pathway.
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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.