ArticleNature communications2023
Tisp40 prevents cardiac ischemia/reperfusion injury through the hexosamine biosynthetic pathway in male mice.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 58 citations in OpenAlex.
- GFPT2 promotes macrophage dysfunction in atherosclerosis via ACADL glycosylation-dependent suppression of ACADL and Arg1.Cellular and molecular life sciences : CMLS · 2026Article
- M6A-modified circArhgap26 attenuates cardiac ischemia‒reperfusion injury by suppressing plakophilin-1 palmitoylation.Signal transduction and targeted therapy · 2026Article
- Fumarate hydratase ameliorates pressure overload induced cardiac remodeling by controlling Elovl7-mediated biosynthesis of unsaturated fatty acids.Acta pharmacologica Sinica · 2026Article
- USP13 ameliorates myocardial infarction injury by inhibiting ferroptosis via stabilizing ALDOA.Redox biology · 2026Article
- O-GlcNAcylation in diabetic cardiac remodeling and a proposed endothelial-macrophage-fibroblast network.Frontiers in immunology · 2026Review
- Dapagliflozin alleviates sunitinib-induced cardiotoxicity through AMPKα-PPARα axis and enhances the sensitivity of renal cell carcinoma to sunitinib.BMC medicine · 2025Article
- Chronic hyperglycemia and cardiovascular dysfunction: an in-depth exploration of metabolic and cellular pathways in type 2 diabetes mellitus.Cardiovascular diabetology. Endocrinology reports · 2025Review
- MEGF9 prevents lipopolysaccharide-induced cardiac dysfunction through activating AMPK pathway.Redox report : communications in free radical research · 2025Article
- Nuclear Receptor Subfamily 4 Group A Member 1 Exacerbates Cardiac Remodeling by Inhibiting Mitochondrial Function Through the Peroxisome Proliferator-Activated Receptor γ Coactivator-1α/Nuclear Respiratory Factor 1/Transcription Factor A Mitochondrial Axis.Journal of the American Heart Association · 2025Article
- Inhibition of AMPKα Pathway by Podocyte GOLM1 Exacerbates Diabetic Nephrology in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Counterbalancing O-GlcNAcylation and STAT3 Phosphorylation in Ventral Tegmental Area Dopaminergic Neurons Mediates Behavioral Adaptations to Acute Restraint Stress.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Role of HINT3 in Myocardial Ischemia-Reperfusion Injury in Male Mice: Mechanisms Involving SDHA and its Acetylation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Exploring the metabolic signaling network of GFPT in cancer.Cell death discovery · 2025Review
- FNDC4 Prevents Aging-Related Cardiac Dysfunction: By Restoring AMPKα/PPARα-Dependent Mitochondrial Function.JACC. Basic to translational science · 2025Article
- Downregulation of Alox5 Inhibits Ferroptosis to Improve Doxorubicin-Induced Cardiotoxicity via the P53/SLC7A11 Pathway.Journal of cellular and molecular medicine · 2025Article
- The efferocytosis process in aging: Supporting evidence, mechanisms, and therapeutic prospects for age-related diseases.Journal of advanced research · 2025Review
- KLF12 Aggravates Angiotensin II-Induced Cardiac Remodeling in Male Mice by Transcriptionally Inhibiting SMAD7.Journal of the American Heart Association · 2025Article
- Activated AXL Ameliorates Alcohol-associated Steatotic Liver Ischemia-Reperfusion Injury by Inhibiting ER stress and Mitochondria-associated Apoptosis.International journal of biological sciences · 2025Article
- FNDC4 alleviates cardiac ischemia/reperfusion injury through facilitating HIF1α-dependent cardiomyocyte survival and angiogenesis in male mice.Nature communications · 2024Article
- Research trends and hotspots of circular RNA in cardiovascular disease: A bibliometric analysis.Non-coding RNA research · 2024Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hexosamine biosynthetic pathway (HBP) produces uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) to facilitate O-linked GlcNAc (O-GlcNAc) protein modifications, and subsequently enhance cell survival under lethal stresses. Transcript induced in spermiogenesis 40 (Tisp40) is an endoplasmic reticulum membrane-resident transcription factor and plays critical roles in cell homeostasis. Here, we show that Tisp40 expression, cleavage and nuclear accumulation are increased by cardiac ischemia/reperfusion (I/R) injury. Global Tisp40 deficiency exacerbates, whereas cardiomyocyte-restricted Tisp40 overexpression ameliorates I/R-induced oxidative stress, apoptosis and acute cardiac injury, and modulates cardiac remodeling and dysfunction following long-term observations in male mice. In addition, overexpression of nuclear Tisp40 is sufficient to attenuate cardiac I/R injury in vivo and in vitro. Mechanistic studies indicate that Tisp40 directly binds to a conserved unfolded protein response element (UPRE) of the glutamine-fructose-6-phosphate transaminase 1 (GFPT1) promoter, and subsequently potentiates HBP flux and O-GlcNAc protein modifications. Moreover, we find that I/R-induced upregulation, cleavage and nuclear accumulation of Tisp40 in the heart are mediated by endoplasmic reticulum stress. Our findings identify Tisp40 as a cardiomyocyte-enriched UPR-associated transcription factor, and targeting Tisp40 may develop effective approaches to mitigate cardiac I/R injury.
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