ArticleCells2022
The ABA-LANCL1/2 Hormone-Receptors System Protects H9c2 Cardiomyocytes from Hypoxia-Induced Mitochondrial Injury via an AMPK- and NO-Mediated Mechanism.
Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Lanthionine synthetase C-like protein 1 (LanCL1): a therapeutic target for neuropathic pain.Pain · 2026Article
- Retinoprotective Effects of Abscisic Acid in Ischemic Retinopathy Mouse Model.Antioxidants (Basel, Switzerland) · 2025Article
- RIPC improves myocardial injury by promoting mitochondrial protection via the PGC-1α/Nrf2 pathway.The Journal of biological chemistry · 2025Article
- Nuclear transport of phosphorylated LanCL2 promotes invadopodia formation and tumor progression of glioblastoma by activating STAT3/Cortactin signaling.Journal of advanced research · 2025Article
- Role of Abscisic Acid in the Whole-Body Regulation of Glucose Uptake and Metabolism.Nutrients · 2024Review
- Thermal measurements support a role of the ABA/LANCL1-2 hormone/receptors system in thermogenesis.Open biology · 2024Article
- The ABA/LANCL1-2 Hormone/Receptors System Controls ROS Production in Cardiomyocytes through ERRα.Biomedicines · 2024Article
- Distinct phenotypes induced by acute hypoxia and TGF-β1 in human adult cardiac fibroblasts.Journal of molecular and cellular cardiology plus · 2024Article
- Genome-Wide Identification and Expression Analysis ofInternational journal of molecular sciences · 2024Article
- New Insights into the LANCL2-Pharmaceutics · 2023Article
- Abscisic Acid and Its Receptors LANCL1 and LANCL2 Control Cardiomyocyte Mitochondrial Function, Expression of Contractile, Cytoskeletal and Ion Channel Proteins and Cell Proliferation via ERRα.Antioxidants (Basel, Switzerland) · 2023Article
- The ABA/LANCL1/2 Hormone/Receptor System Controls Adipocyte Browning and Energy Expenditure.International journal of molecular sciences · 2023Article
- The ABA/LANCL Hormone/Receptor System in the Control of Glycemia, of Cardiomyocyte Energy Metabolism, and in Neuroprotection: A New Ally in the Treatment of Diabetes Mellitus?International journal of molecular sciences · 2023Review
- Amino acid motifs for the identification of novel protein interactants.Computational and structural biotechnology journal · 2023Review
- Evaluation of a large-scale aptamer proteomics platform among patients with kidney failure on dialysis.PloS one · 2023Article
- Identification of miRNAs as Biomarkers of Cardiac Protection in Non-Genetically Modified Primary Human Cardiomyocytes Exposed to Halogenated Hypnotics in an In Vitro Model of Transfection and Ischemia/Reperfusion: A New Model in Translational Anesthesia.Life (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abscisic acid (ABA) regulates plant responses to stress, partly via NO. In mammals, ABA stimulates NO production by innate immune cells and keratinocytes, glucose uptake and mitochondrial respiration by skeletal myocytes and improves blood glucose homeostasis through its receptors LANCL1 and LANCL2. We hypothesized a role for the ABA-LANCL1/2 system in cardiomyocyte protection from hypoxia via NO. The effect of ABA and of the silencing or overexpression of LANCL1 and LANCL2 were investigated in H9c2 rat cardiomyoblasts under normoxia or hypoxia/reoxygenation. In H9c2, hypoxia induced ABA release, and ABA stimulated NO production. ABA increased the survival of H9c2 to hypoxia, and L-NAME, an inhibitor of NO synthase (NOS), abrogated this effect. ABA also increased glucose uptake and NADPH levels and increased phosphorylation of Akt, AMPK and eNOS. Overexpression or silencing of LANCL1/2 significantly increased or decreased, respectively, transcription, expression and phosphorylation of AMPK, Akt and eNOS; transcription of NAMPT, Sirt1 and the arginine transporter. The mitochondrial proton gradient and cell vitality increased in LANCL1/2-overexpressing vs. -silenced cells after hypoxia/reoxygenation, and L-NAME abrogated this difference. These results implicate the ABA-LANCL1/2 hormone-receptor system in NO-mediated cardiomyocyte protection against hypoxia.
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Registered trials
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