ReviewProteomics. Clinical applications2016
Post-translational modifications of the cardiac proteome in diabetes and heart failure.
Review in Proteomics. Clinical applications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 50 citations in OpenAlex.
- Oxidative Modifications in Cardiac Mitochondrial and CaHandbook of experimental pharmacology · 2026Review
- Rg3 regulates myocardial pyruvate metabolism via P300-mediated dihydrolipoamide dehydrogenase 2-hydroxyisobutyrylation in TAC-induced cardiac hypertrophy.Cell death & disease · 2022Article
- Alteration in tyrosine phosphorylation of cardiac proteome and EGFR pathway contribute to hypertrophic cardiomyopathy.Communications biology · 2022Article
- Mitochondrial Fragmentation in a High Homocysteine Environment in Diabetic Retinopathy.Antioxidants (Basel, Switzerland) · 2022Article
- Changes in Protein Structural Motifs upon Post-Translational Modification in Kidney Cancer.Diagnostics (Basel, Switzerland) · 2021Article
- ExcessiveCirculation · 2021Article
- Maintaining Myocardial Glucose Utilization in Diabetic Cardiomyopathy Accelerates Mitochondrial Dysfunction.Diabetes · 2020Article
- Increased Glucose Availability Attenuates Myocardial Ketone Body Utilization.Journal of the American Heart Association · 2020Article
- Basic Mechanisms of Diabetic Heart Disease.Circulation research · 2020Review
- Regulation of cardiac O-GlcNAcylation: More than just nutrient availability.Biochimica et biophysica acta. Molecular basis of disease · 2020Review
- Established and Emerging Mechanisms of Diabetic Cardiomyopathy.Journal of lipid and atherosclerosis · 2019Review
- Clinically Relevant Post-Translational Modification Analyses-Maturing Workflows and Bioinformatics Tools.International journal of molecular sciences · 2018Review
- Of mice and men: models and mechanisms of diabetic cardiomyopathy.Basic research in cardiology · 2018Review
- Glucose transporter 4-deficient hearts develop maladaptive hypertrophy in response to physiological or pathological stresses.American journal of physiology. Heart and circulatory physiology · 2017Article
- Personalized medicine-a modern approach for the diagnosis and management of hypertension.Clinical science (London, England : 1979) · 2017Review
- Diabetes-Related Cardiac Dysfunction.Endocrinology and metabolism (Seoul, Korea) · 2017Review
- Metabolic Origins of Heart Failure.JACC. Basic to translational science · 2017Article
- Cardiovascular consequences of metabolic syndrome.Translational research : the journal of laboratory and clinical medicine · 2017Review
- O-GlcNAcylation and cardiovascular disease.Biochemical Society transactions · 2017Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Cardiovascular complications are the leading cause of death in diabetic patients. Decades of research has focused on altered gene expression, altered cellular signaling, and altered metabolism. This work has led to better understanding of disease progression and treatments aimed at reversing or stopping this deadly process. However, one of the pieces needed to complete the puzzle and bridge the gap between altered gene expression and changes in signaling/metabolism is the proteome and its host of modifications. Defining the mechanisms of regulation includes examining protein levels, localization, and activity of the functional component of cellular machinery. Excess or misutilization of nutrients in obesity and diabetes may lead to PTMs contributing to cardiovascular disease progression. PTMs link regulation of metabolic changes in the healthy and diseased heart with regulation of gene expression itself (e.g. epigenetics), protein enzymatic activity (e.g. mitochondrial oxidative capacity), and function (e.g. contractile machinery). Although a number of PTMs are involved in each of these pathways, we will highlight the role of the serine and threonine O-linked addition of β-N-acetyl-glucosamine or O-GlcNAcylation. This nexus of nutrient supply, utilization, and storage allows for the modification and translation of mitochondrial function to many other aspects of the cell.
Indexed as
Identifiers
What OpenQuestion holds
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.