School of Biomedical Sciences cordially invites you to join the following seminar:

Date: 24 April 2024 (Wednesday)
Time: 4:00 pm – 5:00 pm
Venue: Lecture Theatre 2, G/F, William M.W. Mong Block, 21 Sassoon Road

Speaker: Professor Bent Brachvogel, Head of the Experimental Neonatology, University Childrens Hospital, Cologne, Germany
Talk Title: Mitochondrial dysfunction rewires the TCA cycle to sustain the metabolic flux with detrimental consequences for skeletal aging

Biography

Prof. Dr. Bent Brachvogel is the head of the Experimental Neonatology at the University Childrens Hospital in Cologne. His current research focusses on mitochondria, skeletal development and aging. He aims to unravel how mitochondria dysfunction affects cell metabolism and extracellular matrix (ECM) microenvironment during skeletal development to impair childrens and adult health. Prof. Dr. Bent Brachvogel is also spokesperson of the Research Unit DFG FOR2722 on novel molecular determinants of musculoskeletal diseases (https://for2722.uni-koeln.de/en/). This consortium of researchers with a complementary expertise in basic and translational ECM biology investigates how changes in the ECM affect the function of musculoskeletal tissues and cause connective tissue disorders. His academic journey includes a period as a postdoctoral fellow at the Murdoch Children Research Institute in Melbourne, and a Doctorate in Biology at the University of Erlangen-Nuremberg.

Abstract
Patients suffering from mitochondrial respiratory dysfunction show a broad variety of symptoms but are often described to have a short stature and an aging phenotype. Here we used mutant mice with a cartilage-specific inactivation of the mitochondrial respiratory chain (mtRC) to define the molecular signaling networks that translate mtRC dysfunction into extracellular matrix-dependent skeletal abnormalities. Our analysis showed that mtRC dysfunction is linked to a rewiring of the TCA metabolism leading to an accumulation of amino acids in chondrocytes. These amino acids are sensed by mTORC1-mediated signaling network and translated into enhanced biosynthesis processes, impaired autophagy and ER-stress associated with disturbed extracellular matrix secretion and premature cartilage degradation. The results demonstrate the overall importance of postnatal mtRC activation for skeletal growth and explain why mtRC dysfunction causes premature growth retardation in patients with mitochondrial diseases.

ALL ARE WELCOME

Should you have any enquiries, please feel free to contact Miss Crystal Chan at 3917 6830.