## 1 Introduction  
Glaucoma comprises a group of ocular diseases in which primary open-angle glaucoma (POAG) is the most common form [1]. The disease accompanies various pathophysiological processes that contribute to the apoptosis of retinal ganglion cells (RGCs), leading to vision loss and complete blindness in the patients concerned. Glaucoma is, after age-related macular degeneration, the second leading cause of blindness worldwide, with increasing prevalence [2, 3]. A major risk factor and the only therapeutic target in clinical practice is elevated intraocular pressure (IOP). However, since only about 70% of glaucoma patients possess an elevated IOP, disease progression still occurs in patients despite successful IOP-lowering therapy [4, 5]. Therefore, it is likely that molecular mechanisms underlying RGC loss in addition to high IOP, such as glutamate excitotoxicity, abnormal protein accumulation, vascular dysfunction, and oxidative stress [6, 7, 8, 9, 10]. Increasing IOP can also initiate processes such as oxidative stress [11]. In recent years, oxidative stress has focused more on therapeutic approaches to treat glaucoma [12, 13]. One consequence, especially with prolonged oxidative stress, is the alteration of mitochondrial dynamics which often occurs in other neurodegenerative diseases, such as Alzheimer's (AD) or Parkinson's disease (PD) [14, 15].  
Dynamin-related protein 1 (DRP1) or dynamin-1-like protein (DNM1L) is a small GTPase that regulates mitochondrial dynamics, i.e., fission processes but also indirect fusion processes, to affect the size, shape, and distribution of neurons [16]. Since neuronal cells, in particular, have a high energy demand, fission and fusion must be very tightly regulated. An imbalance of these processes can lead to abnormal structures, leading to mitochondria dysfunctions, such as disturbed ATP production [16]. Consequently, reactive oxygen species (ROS) may increase, leading to the apoptosis of neurons. Dysregulation of DNM1L-dependent mitochondrial fission is associated with neurodegenerative processes in diseases such as AD, Huntington's, PD, or glaucoma [17; 18; 19]. DNM1L activity is modulated by various post-translational modifications (PTMS), such as phosphorylation, ubiquitination, sumoylation, and S-nitrosylation [17; 20]. The pathological imbalance between the DNM1L phosphorylation sites DNM1 Lp635 and DNM1 Lp656 might contribute to the pathogenesis of various neurodegenerative diseases with a special focus on glaucoma [21].  
The present study aimed to investigate the structural and physiological effects of anti-DNM1L Ab injection in a model of chronic IOP elevation. For this purpose, the IOP, the retinal nerve fiber layer thickness (RNFLT), and the retinal functionality were investigated in vivo. In addition, RGC density was determined post-mortem. Changes in DNM1L expression and phosphorylation sites were investigated by western blots, like the expression of the proteins XIAP and BAD, which are involved in mitochondrial apoptosis. In addition, the retinal proteome was analyzed by mass spectrometry to capture the effects of anti-DNM1L Ab treatment in a larger molecular context, which may allow conclusions to be drawn about potential antibody-induced neuroprotective mechanisms. We suggest that intravitreal anti-DNM1L injection may alter DNM1L activity, possibly by changing the ratio of phosphorylation sites, and may cause less apoptosis via the mitochondrial signaling pathway.