ArticleMolecular and cellular biochemistry2015
ZAK induces cardiomyocyte hypertrophy and brain natriuretic peptide expression via p38/JNK signaling and GATA4/c-Jun transcriptional factor activation.
Article in Molecular and cellular biochemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- GATA4-Driven Transcription of HtrA1 Promotes Cellular Senescence in Ménière's Disease and Age-Related Audio-Vestibular Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Rutin Alleviates Oxidative Stress in Chicken Hepatocytes by Inhibiting Ribotoxic Stress Response.Animals : an open access journal from MDPI · 2026Article
- ZAK kinase at the crossroads of cellular stress: functional plasticity, human pathobiology, and precision therapeutics.Frontiers in cell and developmental biology · 2026Review
- In Silico, In Vitro, and In Vivo Evaluation of Woodfordia Fruticosa for Cardio Protection against Doxorubicin-Induced Cardiomyopathy.Chemistry & biodiversity · 2026Article
- ZAKβ Alleviates Oxidized Low-density Lipoprotein (ox-LDL)-Induced Apoptosis and B-type Natriuretic Peptide (BNP) Upregulation in Cardiomyoblast.Cell biochemistry and biophysics · 2022Article
- Long non-coding RNA MIAT regulates blood tumor barrier permeability by functioning as a competing endogenous RNA.Cell death & disease · 2020Article
- SUMO proteins in the cardiovascular system: friend or foe?Journal of biomedical science · 2020Review
- Molecular Mechanisms of Adiponectin-Induced Attenuation of Mechanical Stretch-Mediated Vascular Remodeling.Oxidative medicine and cellular longevity · 2020Article
- Recessive mutations in the kinase ZAK cause a congenital myopathy with fibre type disproportion.Brain : a journal of neurology · 2017Article
- The Role of p38 MAPK in the Development of Diabetic Cardiomyopathy.International journal of molecular sciences · 2016Review
- Structure of the Human Protein Kinase ZAK in Complex with Vemurafenib.ACS chemical biology · 2016Article
- Activation of the Classical Mitogen-Activated Protein Kinases Is Part of the Shiga Toxin-Induced Ribotoxic Stress Response and May Contribute to Shiga Toxin-Induced Inflammation.Infection and immunity · 2016Article
- Calcineurin/NFAT Activation-Dependence of Leptin Synthesis and Vascular Growth in Response to Mechanical Stretch.Frontiers in physiology · 2016Article
- Mechanical stretch-induced vascular hypertrophy occurs through modulation of leptin synthesis-mediated ROS formation and GATA-4 nuclear translocation.Frontiers in pharmacology · 2015Article
Corrections and comments
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Authors and funding
10 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiomyocyte hypertrophy is an adaptive response of heart to various stress conditions. During the period of stress accumulation, transition from physiological hypertrophy to pathological hypertrophy results in the promotion of heart failure. Our previous studies found that ZAK, a sterile alpha motif and leucine zipper containing kinase, was highly expressed in infarcted human hearts and demonstrated that overexpression of ZAK induced cardiac hypertrophy. This study evaluates, cellular events associated with the expression of two doxycycline (Dox) inducible Tet-on ZAK expression systems, a Tet-on ZAK WT (wild-type), and a Tet-on ZAK DN (mutant, Dominant-negative form) in H9c2 myoblast cells; Tet-on ZAK WT was found to increase cell size and hypertrophic marker BNP in a dose-dependent manner. To ascertain the mechanism of ZAK-mediated hypertrophy, expression analysis with various inhibitors of the related upstream and downstream proteins was performed. Tet-on ZAK WT expression triggered the p38 and JNK pathway and also activated the expression and nuclear translocation of p-GATA4 and p-c-Jun transcription factors, without the involvement of p-ERK or NFATc3. However, Tet-on ZAK DN showed no effect on the p38 and JNK signaling cascade. The results showed that the inhibitors of JNK1/2 and p38 significantly suppressed ZAK-induced BNP expression. The results show the role of ZAK and/or the ZAK downstream events such as JNK and p38 phosphorylation, c-Jun, and GATA-4 nuclear translocation in cardiac hypertrophy. ZAK and/or the ZAK downstream p38, and JNK pathway could therefore be potential targets to ameliorate cardiac hypertrophy symptoms in ZAK-overexpressed patients.
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