About

E. Dale Abel is a Professor and Department Chair of Medicine at UCLA. His research activities and funding focus on molecular determinants of heart structure and function, modulation of reactive oxygen species (ROS) to treat type 2 diabetes, and the role of mitochondrial proteins such as OPA1 and MG53 in cardiovascular health. His work includes investigating insulin signaling, cardiac dysfunction in metabolic syndrome, and the impact of various molecular pathways on cardiovascular diseases related to diabetes. Abel has contributed significantly to understanding the intersection of metabolism, cardiovascular health, and diabetes, with numerous projects supported by NIH grants. His research aims to elucidate mechanisms underlying diabetic cardiomyopathy, mitochondrial function, and metabolic regulation in the heart.

Research topics

• Endocrinology
• Medicine
• Internal medicine
• Chemistry
• Biochemistry
• Biology
• Cardiology
• Cell biology

Selected publications

• Functional resilience of C57BL/6J mouse heart to dietary fat overload

  AJP Heart and Circulatory Physiology · 2021 · 21 citations

  Senior authorCorresponding
  • Internal medicine
  • Cardiology
  • Endocrinology

  Dietary fat overload (DFO) is widely used to model diabetic cardiomyopathy but the utility of this model is controversial. We comprehensively characterized cardiac contractile and mitochondrial function in C57BL6/J mice fed with lard-based or saturated fat-enriched diets initiated at two ages. Despite cardiac hypertrophy, contractile and mitochondrial function is preserved, and molecular adaptations likely limit lipotoxicity. The resilience of these hearts to DFO underscores the need to develop robust alternative models of diabetic cardiomyopathy.

  DOI

• Mitochondrial pyruvate carriers are required for myocardial stress adaptation

  Nature Metabolism · 2020 · 143 citations

  Senior authorCorresponding
  • Internal medicine
  • Endocrinology
  • Biology
  DOI

• The Role of Nonglycolytic Glucose Metabolism in Myocardial Recovery Upon Mechanical Unloading and Circulatory Support in Chronic Heart Failure

  Circulation · 2020 · 81 citations

  • Medicine
  • Internal medicine
  • Biochemistry

  BACKGROUND: Significant improvements in myocardial structure and function have been reported in some patients with advanced heart failure (termed responders [R]) following left ventricular assist device (LVAD)-induced mechanical unloading. This therapeutic strategy may alter myocardial energy metabolism in a manner that reverses the deleterious metabolic adaptations of the failing heart. Specifically, our previous work demonstrated a post-LVAD dissociation of glycolysis and oxidative-phosphorylation characterized by induction of glycolysis without subsequent increase in pyruvate oxidation through the tricarboxylic acid cycle. The underlying mechanisms responsible for this dissociation are not well understood. We hypothesized that the accumulated glycolytic intermediates are channeled into cardioprotective and repair pathways, such as the pentose-phosphate pathway and 1-carbon metabolism, which may mediate myocardial recovery in R. METHODS: We prospectively obtained paired left ventricular apical myocardial tissue from nonfailing donor hearts as well as R and nonresponders at LVAD implantation (pre-LVAD) and transplantation (post-LVAD). We conducted protein expression and metabolite profiling and evaluated mitochondrial structure using electron microscopy. RESULTS: Western blot analysis shows significant increase in rate-limiting enzymes of pentose-phosphate pathway and 1-carbon metabolism in post-LVAD R (post-R) as compared with post-LVAD nonresponders (post-NR). The metabolite levels of these enzyme substrates, such as sedoheptulose-6-phosphate (pentose phosphate pathway) and serine and glycine (1-carbon metabolism) were also decreased in Post-R. Furthermore, post-R had significantly higher reduced nicotinamide adenine dinucleotide phosphate levels, reduced reactive oxygen species levels, improved mitochondrial density, and enhanced glycosylation of the extracellular matrix protein, α-dystroglycan, all consistent with enhanced pentose-phosphate pathway and 1-carbon metabolism that correlated with the observed myocardial recovery. CONCLUSIONS: The recovering heart appears to direct glycolytic metabolites into pentose-phosphate pathway and 1-carbon metabolism, which could contribute to cardioprotection by generating reduced nicotinamide adenine dinucleotide phosphate to enhance biosynthesis and by reducing oxidative stress. These findings provide further insights into mechanisms responsible for the beneficial effect of glycolysis induction during the recovery of failing human hearts after mechanical unloading.

  DOI

• Basic Mechanisms of Diabetic Heart Disease

  Circulation Research · 2020 · 688 citations

  Senior authorCorresponding
  • Medicine
  • Cardiology
  • Internal medicine

  Diabetes mellitus predisposes affected individuals to a significant spectrum of cardiovascular complications, one of the most debilitating in terms of prognosis is heart failure. Indeed, the increasing global prevalence of diabetes mellitus and an aging population has given rise to an epidemic of diabetes mellitus-induced heart failure. Despite the significant research attention this phenomenon, termed diabetic cardiomyopathy, has received over several decades, understanding of the full spectrum of potential contributing mechanisms, and their relative contribution to this heart failure phenotype in the specific context of diabetes mellitus, has not yet been fully resolved. Key recent preclinical discoveries that comprise the current state-of-the-art understanding of the basic mechanisms of the complex phenotype, that is, the diabetic heart, form the basis of this review. Abnormalities in each of cardiac metabolism, physiological and pathophysiological signaling, and the mitochondrial compartment, in addition to oxidative stress, inflammation, myocardial cell death pathways, and neurohumoral mechanisms, are addressed. Further, the interactions between each of these contributing mechanisms and how they align to the functional, morphological, and structural impairments that characterize the diabetic heart are considered in light of the clinical context: from the disease burden, its current management in the clinic, and where the knowledge gaps remain. The need for continued interrogation of these mechanisms (both known and those yet to be identified) is essential to not only decipher the how and why of diabetes mellitus-induced heart failure but also to facilitate improved inroads into the clinical management of this pervasive clinical challenge.

  DOI

• Exposure to Static Magnetic and Electric Fields Treats Type 2 Diabetes

  Cell Metabolism · 2020 · 81 citations

  • Medicine
  • Chemistry
  • Cell biology
  DOI

Recent grants

• NIH Grant P30HL101310

  NIH · $839k · 2012

• NIH Grant R21HL062886

  NIH · $348k · 2000

• NIH Grant R01HL108379

  NIH · $1.5M · 2017

• NIH Grant R03DK058073

  NIH · $167k · 2003

• Interdisciplinary Training Program in Metabolism

  NIH · $4.5M · 2011–2026

Frequent coauthors

• Renata O. Pereira

  Fraternal Order of Eagles

  206 shared

• Adam R. Wende

  University of Alabama at Birmingham

  196 shared

• Christian Riehle

  Medizinische Hochschule Hannover

  156 shared

• Yuan Zhang

  Fraternal Order of Eagles

  141 shared

• Jamie Soto

  133 shared

• Heiko Bugger

  Medical University of Graz

  131 shared

• Rhonda Souvenir

  UCLA Health

  108 shared

• Crystal Sloan

  Fraternal Order of Eagles

  85 shared

Education

• PhD

  Oxford University

  1991

• MBBS

  University of the West Indies

  1985

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