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Revolutionary research against glaucoma: Mainz and Sydney in close contact
The University of Mainz is collaborating with Sydney to develop new treatments for glaucoma and combat vision loss.
Revolutionary research against glaucoma: Mainz and Sydney in close contact
On July 1, 2025, Mainz University Medical Center joined a global research collaboration dedicated to combating vision loss caused by glaucoma. This collaboration is led by Univ.-Prof. Christian Behl, Director of the Institute for Pathobiochemistry, led. Together with Dr. Katharina Bell, clinical lead in ophthalmology at the NHMRC Clinical Trials Center at the University of Sydney, is committed to developing innovative treatment options for patients with glaucoma. unimedizin-mainz.de reports that the project is part of the “Snow Vision Accelerator” network, which has an extraordinarily high budget of 27.9 million euros and is led by Prof. Jonathan Crowston. Funding is provided by the “Snow Medical Research Foundation” from Sydney.
The central goal of this pioneering initiative is to revolutionize glaucoma treatment. This will be done through molecular biological, genetic and translational research in order to develop novel drugs. Glaucoma, also known as glaucoma, often leads to damage to the optic nerve, which in turn can lead to visual field restrictions and blind spots for those affected. A common feature of this condition is increased intraocular pressure.
Research focus and methodology
In their research, Behl and Bell focus on autophagy, particularly mitophagy, which is responsible for the breakdown of mitochondria. Around 1.3 million euros will be available for these studies over the next five years. Autophagy plays an important role in cellular quality control and energy production and is crucial in stress responses.
The identification of new therapeutic approaches to preserve and protect the optic nerve through targeted control of mitophagy is a central concern of this collaboration. The study of these processes is particularly important because mitochondrial dysfunction plays a role in the pathogenesis of primary open-angle glaucoma (POAG). pubmed.ncbi.nlm.nih.gov highlights that mTOR and AMPK are the main regulators of autophagy, with mTOR acting as a negative regulator and AMPK as a positive regulator.
In particular, the ULK1/ATG13/FIP200 complex is considered central to the formation of autophagosomes, while key proteins such as BECN1, PI3K and ATG14L are crucial for autophagosome elongation. The ability of mitochondria to respond to stress signals such as reactive oxygen species leads to the activation of the mitophagy process, which ultimately affects the mitochondria.
Genetic influences and therapeutic perspectives
Additionally, current research is deepening our understanding of the genetic influences on mitochondrial dysfunction and its connection to retinal ganglion cell loss in POAG. pubmed.ncbi.nlm.nih.gov documented that changes in mitochondrial DNA and nuclear DNA genes that encode mitochondrial proteins can have significant effects on mitochondrial structure and function.
A variety of genes, including OPA1, MFN1, and SOD2, are associated with susceptibility to POAG. These genotypic variations reveal a common denominator regarding mitochondrial dysfunction, highlighting the need to explore deeper therapeutic interventions.
Dr. Katharina Bell is optimistic about the collaboration and the opportunity to positively influence the lives of people with glaucoma. The interdisciplinary approach between neuroscience and ophthalmology aims to develop new treatment strategies.