Wolfgang Dillmann

About

Wolfgang Dillmann is a faculty member at UCSD in the School of Medicine, with research activities focused on heart function, aging, and related cardiovascular conditions. His work involves investigating the molecular mechanisms underlying heart failure, diabetic cardiomyopathy, and cardiac hypertrophy, with particular attention to mitochondrial calcium handling, protein O-GlcNAcylation, and the role of thyroid hormone receptors in cardiac health. His research has contributed to understanding how mitochondrial dysfunction, oxidative stress, and metabolic regulation impact heart disease, especially in the context of diabetes and aging. Throughout his career, Dr. Dillmann has led numerous NIH-funded projects as Principal Investigator, exploring topics such as heart vascular function, thyroid hormone action in the heart, and mitochondrial calcium regulation. His studies employ experimental endocrinology, molecular biology, and physiology to elucidate the pathways involved in cardiac pathophysiology. His work has advanced knowledge on the molecular and cellular basis of heart failure, with implications for developing targeted therapies for cardiovascular diseases related to metabolic and age-related factors.

Research topics

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

Selected publications

• Diabetic Cardiomyopathy

  Circulation Research · 2019-04-11 · 657 citations

  reviewOpen access1st authorCorresponding

  Diabetic cardiomyopathy was initially described as a human pathophysiological condition in which heart failure occurred in the absence of coronary artery disease, hypertension, and valvular heart disease. Recent studies in diabetic animal models identify decreased cardiomyocyte function as an important mediating mechanism for heart failure. Decreased cardiomyocyte function is in part mediated by abnormal mitochondrial calcium handling and a decreased level of free matrix calcium levels which cou…

  PublisherOA PDFDOI

• Restoring mitochondrial calcium uniporter expression in diabetic mouse heart improves mitochondrial calcium handling and cardiac function

  Journal of Biological Chemistry · 2018-04-06 · 101 citations

  articleOpen accessSenior authorCorresponding

  handling and its negative consequences can be ameliorated in diabetes by restoring MCU levels via adeno-associated virus-based MCU transgene expression.

  PublisherOA PDFDOI

• Maintaining Myocardial Glucose Utilization in Diabetic Cardiomyopathy Accelerates Mitochondrial Dysfunction

  Diabetes · 2020-05-04 · 70 citations

  letterOpen access

  Cardiac glucose uptake and oxidation are reduced in diabetes despite hyperglycemia. Mitochondrial dysfunction contributes to heart failure in diabetes. It is unclear whether these changes are adaptive or maladaptive. To directly evaluate the relationship between glucose delivery and mitochondrial dysfunction in diabetic cardiomyopathy, we generated transgenic mice with inducible cardiomyocyte-specific expression of the GLUT4. We examined mice rendered hyperglycemic following low-dose streptozoto…

  PublisherOA PDFDOI

• Expression of the mitochondrial calcium uniporter in cardiac myocytes improves impaired mitochondrial calcium handling and metabolism in simulated hyperglycemia

  American Journal of Physiology-Cell Physiology · 2016-09-29 · 69 citations

  articleOpen accessSenior authorCorresponding

  Diabetic cardiomyopathy is associated with metabolic changes, including decreased glucose oxidation (Gox) and increased fatty acid oxidation (FAox), which result in cardiac energetic deficiency. Diabetic hyperglycemia is a pathophysiological mechanism that triggers multiple maladaptive phenomena. The mitochondrial Ca 2+ uniporter (MCU) is the channel responsible for Ca 2+ uptake in mitochondria, and free mitochondrial Ca 2+ concentration ([Ca 2+ ] m ) regulates mitochondrial metabolism. Experime…

  PublisherOA PDFDOI

• Protein Kinase G Activation Reverses Oxidative Stress and Restores Osteoblast Function and Bone Formation in Male Mice With Type 1 Diabetes

  Diabetes · 2018-01-04 · 67 citations

  articleOpen access

  Bone loss and fractures are underrecognized complications of type 1 diabetes and are primarily due to impaired bone formation by osteoblasts. The mechanisms leading to osteoblast dysfunction in diabetes are incompletely understood, but insulin deficiency, poor glycemic control, and hyperglycemia-induced oxidative stress likely contribute. Here we show that insulin promotes osteoblast proliferation and survival via the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP)/protein kinase G (PKG)…

  PublisherOA PDFDOI

Recent grants

• NIH Grant R37HL049434

  NIH · $3.1M · 2008

• NIH Grant R01HL066917

  NIH · $4.8M · 2013

• NIH Grant R01HL049434

  NIH · $1.2M · 1998

Frequent coauthors

• Jorge Suárez

  Veterans Medical Research Foundation of San Diego

  65 shared

• Brian T. Scott

  University of California System

  46 shared

• Ruben Mestril

  University of Chicago

  36 shared

• Patrick M. McDonough

  Andrew McDonough B+ Foundation

  30 shared

• Darrell D. Belke

  University of Calgary

  27 shared

• Ayako Makino

  University of Arizona

  26 shared

• Jack H. Oppenheimer

  University of Minnesota

  24 shared

• Markus Meyer

  Minneapolis Heart Institute Foundation

  23 shared

Similar researchers at University of California, San Diego

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• Alan Saltielh-112