ArticleNature communications2017
Snf1-related kinase improves cardiac mitochondrial efficiency and decreases mitochondrial uncoupling.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- TRIB3 Promotes Laryngeal Cancer Progression via Regulating Ubiquitination of PPARα.Biochemical genetics · 2026Article
- Exploring the Phosphoregulatory Network of Human Sucrose Non-Fermenting 1-Related Kinase.Biology · 2026Article
- Predictive value of TRIB3 combined with BMPR2 for major adverse cardiovascular events in elderly coronary heart disease patients undergoing percutaneous coronary intervention.Journal of medical biochemistry · 2026Article
- Smooth muscle cell (SMC)-Specific SNRK deletion in mouse causes congenital short bowel syndrome and premature death.Biochemistry and biophysics reports · 2025Article
- SNRK facilitates cardiac repair associated with nonischemic fibrosis: regulating transforming growth factor-beta1 levels in atrial cardiomyocytes.Regenerative medicine reports · 2025Article
- ATP homeostasis and signaling in plants.Plant communications · 2024Review
- DNA Damage and Nuclear Morphological Changes in Cardiac Hypertrophy Are Mediated by SNRK Through Actin Depolymerization.Circulation · 2023Article
- Article
- DNA damage and nuclear morphological changes in cardiac hypertrophy are mediated by SNRK through actin depolymerization.bioRxiv : the preprint server for biology · 2023Article
- Thrombus-specific/responsive biomimetic nanomedicine for spatiotemporal thrombolysis and alleviation of myocardial ischemia/reperfusion injury.Journal of nanobiotechnology · 2022Article
- Overexpression of circRNA SNRK targets miR-103-3p to reduce apoptosis and promote cardiac repair through GSK3β/β-catenin pathway in rats with myocardial infarction.Cell death discovery · 2021Article
- Article
- DHA Supplementation Attenuates MI-Induced LV Matrix Remodeling and Dysfunction in Mice.Oxidative medicine and cellular longevity · 2020Article
- Cardiomyocyte-SpecificJournal of the American Heart Association · 2019Article
- Dysregulation of PP2A-Akt interaction contributes to Sucrose non-fermenting related kinase (SNRK) deficiency induced insulin resistance in adipose tissue.Molecular metabolism · 2019Article
- Circulating miR-103a-3p contributes to angiotensin II-induced renal inflammation and fibrosis via a SNRK/NF-κB/p65 regulatory axis.Nature communications · 2019Article
- Sucrose Nonfermenting-Related Kinase Regulates Both Adipose Inflammation and Energy Homeostasis in Mice and Humans.Diabetes · 2018Article
- SNRK (Sucrose Nonfermenting 1-Related Kinase) Promotes Angiogenesis In Vivo.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Ischaemic heart disease limits oxygen and metabolic substrate availability to the heart, resulting in tissue death. Here, we demonstrate that the AMP-activated protein kinase (AMPK)-related protein Snf1-related kinase (SNRK) decreases cardiac metabolic substrate usage and mitochondrial uncoupling, and protects against ischaemia/reperfusion. Hearts from transgenic mice overexpressing SNRK have decreased glucose and palmitate metabolism and oxygen consumption, but maintained power and function. They also exhibit decreased uncoupling protein 3 (UCP3) and mitochondrial uncoupling. Conversely, Snrk knockout mouse hearts have increased glucose and palmitate oxidation and UCP3. SNRK knockdown in cardiac cells decreases mitochondrial efficiency, which is abolished with UCP3 knockdown. We show that Tribbles homologue 3 (Trib3) binds to SNRK, and downregulates UCP3 through PPARα. Finally, SNRK is increased in cardiomyopathy patients, and SNRK reduces infarct size after ischaemia/reperfusion. SNRK also decreases cardiac cell death in a UCP3-dependent manner. Our results suggest that SNRK improves cardiac mitochondrial efficiency and ischaemic protection.
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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.