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Moritz Brandt

Cardiovascular ageing – the role of telomere shortening, inflammation and reactive oxygen species (ROS)

We are facing dramatically rising numbers of patients of increasing age. Efforts and costs are increasing, while funds and resources are limited. Ageing is the main risk factor for cardiovascular diseases, which are the most common cause of morbidity, mortality and associated healthcare costs globally. More specifically, heart failure (HF) resulting from acute or chronic myocardial ischemia is the most common cause of death; it is responsible for 16% of deaths worldwide, with the highest increments occurring since the beginning of the 21st century, and its prevalence increases dramatically with age. We need novel approaches to improve HF treatment and prevention.

Towards this end, we and others could show that telomere shortening occurs universally in HF and is mechanistically linked to its fundamental pathomechanisms.

We investigate:

  • The mechanisms underlying ROS-induced damage of (telomeric) DNA in HF.
  • Cellular and functional sequelae of cardiovascular telomere shortening.
  • The role of accumulating defective DNA repair and accumulating ribonucleotide insertions in HF.

Positions held

  • Since 2024: Advanced Clinician Scientist funded by CHANCE, University Medical Center (UMC) and Institute of Molecular Biology (IMB), Mainz
  • Since 2018: Consulting physician, general and interventional cardiology
  • 2012 - 2014: Postdoctoral researcher, Stanford University, USA
  • 2009 - 2020: Residency, Fellowship for Interventional Cardiology, Center for Cardiology, University Medical Center (UMC) Mainz

Education

  • 2011: MD, University Medical Center (UMC) Mainz (summa cum laude)
  • 2003 - 2009: Medical Studies, Johannes Gutenberg University (JGU), Mainz

Selected publications by Moritz Brandt

Brandt M, Dorschmann H, Khraisat S, Knopp T, Ringen J, Kalinovic S, Garlapati V, Siemer S, Molitor M, Gobel S, Stauber R, Karbach SH, Munzel T, Daiber A and Wenzel P (2022) Telomere shortening in hypertensive heart disease depends on oxidative DNA damage and predicts impaired recovery of cardiac function in heart failure. Hypertension, 79(10):2173-2184 Link

Brandt M, Giokoglu E, Garlapati V, Bochenek ML, Molitor M, Hobohm L, Schonfelder T, Munzel T, Kossmann S, Karbach SH, Schafer K and Wenzel P (2018) Pulmonary arterial hypertension and endothelial dysfunction is linked to NADPH oxidase-derived superoxide formation in venous thrombosis and pulmonary embolism in mice. Oxid Med Cell Longev, 2018:1860513 Link

Brandt M, Garlapati V, Oelze M, Sotiriou E, Knorr M, Kroller-Schon S, Kossmann S, Schonfelder T, Morawietz H, Schulz E, Schultheiss HP, Daiber A, Munzel T and Wenzel P (2016) NOX2 amplifies acetaldehyde-mediated cardiomyocyte mitochondrial dysfunction in alcoholic cardiomyopathy.Sci Rep, 6:32554 Link

Ramunas J, Yakubov E, Brady JJ, Corbel SY, Holbrook C, Brandt M, Stein J, Santiago JG, Cooke JP and Blau HM (2015) Transient delivery of modified mRNA encoding TERT rapidly extends telomeres in human cells.FASEB J, 29(5):1930-1939 Link