Julia Ritterhoff
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View article: Cardiac-Targeted AAV5-S100A1 Gene Therapy Protects Against Adverse Remodeling and Contractile Dysfunction in Postischemic Hearts
Cardiac-Targeted AAV5-S100A1 Gene Therapy Protects Against Adverse Remodeling and Contractile Dysfunction in Postischemic Hearts Open
BACKGROUND: Guided by long-term safety data for AAV5 (adeno-associated virus 5) in humans, our translational study investigated whether AAV5 effectively delivers genes to healthy and achieves therapeutic efficacy in dysfunctional human-siz…
View article: <sup>13</sup>C stable isotope tracing reveals distinct fatty acid oxidation pathways in proliferative versus oxidative cells
<sup>13</sup>C stable isotope tracing reveals distinct fatty acid oxidation pathways in proliferative versus oxidative cells Open
By using 13 C stable isotope-resolved metabolomics and FA-driven oxygen consumption rate analysis, our study provides novel insights into the fate of FA carbon through β-oxidation and downstream TCA cycle in proliferative and oxidative cel…
View article: S100A1ct: A Synthetic Peptide Derived From S100A1 Protein Improves Cardiac Performance and Survival in Preclinical Heart Failure Models
S100A1ct: A Synthetic Peptide Derived From S100A1 Protein Improves Cardiac Performance and Survival in Preclinical Heart Failure Models Open
BACKGROUND: The EF-hand Ca 2+ sensor protein S100A1 has been identified as a molecular regulator and enhancer of cardiac performance. The ability of S100A1 to recognize and modulate the activity of targets such as SERCA2a (sarcoplasmic ret…
View article: Editorial: Mitochondrial dysfunction affects mechano-energetic coupling in heart failure
Editorial: Mitochondrial dysfunction affects mechano-energetic coupling in heart failure Open
Citation: Dudek J and Ritterhoff J (2024) Editorial: Mitochondrial dysfunction affects mechano-energetic coupling in heart failure. Front. Mol. Med. 4:1433102. doi: 10.3389/fmmed.2024.1433102
View article: S100A1’s single cysteine is an indispensable redox switch for the protection against diastolic calcium waves in cardiomyocytes
S100A1’s single cysteine is an indispensable redox switch for the protection against diastolic calcium waves in cardiomyocytes Open
S100A1 is an emerging candidate for future gene-therapy treatment of human chronic heart failure. We aimed to study the significance of the conserved single-cysteine 85 (C85) residue in cardiomyocytes. We show that S100A1 is endogenously g…
View article: S100A1: a promising therapeutic target for heart failure
S100A1: a promising therapeutic target for heart failure Open
View article: Raising NAD <sup>+</sup> Level Stimulates Short-Chain Dehydrogenase/Reductase Proteins to Alleviate Heart Failure Independent of Mitochondrial Protein Deacetylation
Raising NAD <sup>+</sup> Level Stimulates Short-Chain Dehydrogenase/Reductase Proteins to Alleviate Heart Failure Independent of Mitochondrial Protein Deacetylation Open
BACKGROUND: Strategies to increase cellular NAD + (oxidized nicotinamide adenine dinucleotide) level have prevented cardiac dysfunction in multiple models of heart failure, but molecular mechanisms remain unclear. Little is known about the…
View article: S100A1’s single cysteine is an indispensable redox-switch for the protection against diastolic calcium leakage in cardiomyocytes
S100A1’s single cysteine is an indispensable redox-switch for the protection against diastolic calcium leakage in cardiomyocytes Open
The EF-hand calcium (Ca 2+ ) sensor protein S100A1 combines inotropic with antiarrhythmic potency in cardiomyocytes (CM). Oxidative posttranslational modification (ox-PTM) of S100A1’s conserved, single cysteine residue (C85) via reactive n…
View article: Branched-chain keto acids inhibit mitochondrial pyruvate carrier and suppress gluconeogenesis in hepatocytes
Branched-chain keto acids inhibit mitochondrial pyruvate carrier and suppress gluconeogenesis in hepatocytes Open
Branched-chain amino acid (BCAA) metabolism is linked to glucose homeostasis, but the underlying signaling mechanisms are unclear. We find that gluconeogenesis is reduced in mice deficient of Ppm1k, a positive regulator of BCAA catabolism,…
View article: 105 Burning Heart - An Animal Model of Chronic Heart Failure Following Severe Burn Injury
105 Burning Heart - An Animal Model of Chronic Heart Failure Following Severe Burn Injury Open
Introduction Our clinical research unveiled chronic heart failure with preserved ejection fraction (HFpEF) as a long-term sequel in survivors of severe pediatric burn injury due to a yet unknown molecular pathomechanism. Applying a standar…
View article: Cardiac-targeted rAAV5-S100A1 gene therapy protects against adverse remodeling and contractile dysfunction in post-ischemic hearts
Cardiac-targeted rAAV5-S100A1 gene therapy protects against adverse remodeling and contractile dysfunction in post-ischemic hearts Open
Summary Toxicity by recombinant adeno-associated viruses (rAAV) in clinical gene therapy trials (e.g., by rAAV9-mediated fatal liver failure) significantly impairs translation of preclinical rAAV-based cardiac gene therapies employing thes…
View article: S100A1ct: a synthetic peptide derived from human S100A1 protein improves cardiac contractile performance and survival in pre-clinical heart failure models
S100A1ct: a synthetic peptide derived from human S100A1 protein improves cardiac contractile performance and survival in pre-clinical heart failure models Open
Background The EF-hand Ca 2+ sensor protein S100A1 has been identified as a molecular regulator and enhancer of cardiac performance. S100A1’s ability to recognize and modulate the activity of targets such as SERCA2a and RyR2 in cardiomyocy…
View article: SUMO interacting motif (SIM) of S100A1 is critical for S100A1 post-translational protein stability
SUMO interacting motif (SIM) of S100A1 is critical for S100A1 post-translational protein stability Open
S100A1 is a small EF-type Ca 2+ sensor protein that belongs to the multigenic S100 protein family. It is abundantly expressed in cardiomyocytes (CMs) and has been described as a key regulator of CM performance due to its unique ability to …
View article: Upregulation of mitochondrial ATPase inhibitory factor 1 (ATPIF1) mediates increased glycolysis in mouse hearts
Upregulation of mitochondrial ATPase inhibitory factor 1 (ATPIF1) mediates increased glycolysis in mouse hearts Open
In hypertrophied and failing hearts, fuel metabolism is reprogrammed to increase glucose metabolism, especially glycolysis. This metabolic shift favors biosynthetic function at the expense of ATP production. Mechanisms responsible for the …
View article: Branched-Chain Keto Acid Inhibits Mitochondrial Pyruvate Carrier and Suppresses Gluconeogenesis
Branched-Chain Keto Acid Inhibits Mitochondrial Pyruvate Carrier and Suppresses Gluconeogenesis Open
View article: Increasing fatty acid oxidation elicits a sex-dependent response in failing mouse hearts
Increasing fatty acid oxidation elicits a sex-dependent response in failing mouse hearts Open
View article: Metabolic Remodeling Promotes Cardiac Hypertrophy by Directing Glucose to Aspartate Biosynthesis
Metabolic Remodeling Promotes Cardiac Hypertrophy by Directing Glucose to Aspartate Biosynthesis Open
Rationale: Hypertrophied hearts switch from mainly using fatty acids (FAs) to an increased reliance on glucose for energy production. It has been shown that preserving FA oxidation (FAO) prevents the pathological shift of substrate prefere…
View article: Fatty Acids Enhance the Maturation of Cardiomyocytes Derived from Human Pluripotent Stem Cells
Fatty Acids Enhance the Maturation of Cardiomyocytes Derived from Human Pluripotent Stem Cells Open
Although human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) have emerged as a novel platform for heart regeneration, disease modeling, and drug screening, their immaturity significantly hinders their application. A hallmark of p…
View article: Glucose promotes cell growth by suppressing branched-chain amino acid degradation
Glucose promotes cell growth by suppressing branched-chain amino acid degradation Open
Glucose and branched-chain amino acids (BCAAs) are essential nutrients and key determinants of cell growth and stress responses. High BCAA level inhibits glucose metabolism but reciprocal regulation of BCAA metabolism by glucose has not be…
View article: Metabolism in cardiomyopathy: every substrate matters
Metabolism in cardiomyopathy: every substrate matters Open
Cardiac metabolism is highly adaptive to changes in fuel availability and the energy demand of the heart. This metabolic flexibility is key for the heart to maintain its output during the development and in response to stress. Alterations …
View article: Defective Branched-Chain Amino Acid Catabolism Disrupts Glucose Metabolism and Sensitizes the Heart to Ischemia-Reperfusion Injury
Defective Branched-Chain Amino Acid Catabolism Disrupts Glucose Metabolism and Sensitizes the Heart to Ischemia-Reperfusion Injury Open
View article: S100A1 DNA-based Inotropic Therapy Protects Against Proarrhythmogenic Ryanodine Receptor 2 Dysfunction
S100A1 DNA-based Inotropic Therapy Protects Against Proarrhythmogenic Ryanodine Receptor 2 Dysfunction Open
View article: Cardiomyocytes, Endothelial Cells and Cardiac Fibroblasts: S100A1’s Triple Action in Cardiovascular Pathophysiology
Cardiomyocytes, Endothelial Cells and Cardiac Fibroblasts: S100A1’s Triple Action in Cardiovascular Pathophysiology Open
Over the past decade, basic and translational research delivered comprehensive evidence for the relevance of the Ca(2+)-binding protein S100A1 in cardiovascular diseases. Aberrant expression levels of S100A1 surfaced as molecular key defec…