ArticlebioRxiv : the preprint server for biology2025
Developmental wave of programmed ganglion cell death in human retinal organoids.
Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
The delicate and complex structure of the neural retina that enables proper visual function is achieved during embryonic development through a precise balance of proliferation, differentiation, and cell death. Retinal ganglion cells (RGC), the only output neurons of the retina, show a steady increase in numbers during development except for two waves of cell death that are highly conserved in vertebrates. However, the mechanisms responsible for these phenomena and their conservation in the human retina are incompletely understood. In this work we took advantage of human induced pluripotent stem cell (hiPSC)-derived retinal organoids to explore these questions. Using different markers and quantitative techniques in three different hiPSC lines, we found a consistent decrease in RGC numbers at week 8 of differentiation, a developmental stage that is equivalent to that of the first wave of RGC death in other species. This decrease coincided with a peak in caspase 3 activation and TUNEL(+) staining, suggesting an apoptotic mechanism. Notably, this was accompanied by a decrease in the BAX/BCL2 ratio and a lack of caspase 9 activation. However, we observed a marked increase in caspase 8 activation at this stage, suggesting the involvement of the extrinsic apoptotic pathway. Together, these results show for the first time the intrinsic ability of the human retina to regulate RGC numbers through programmed cell death mechanisms, which could lead to new insights regarding congenital retinal abnormalities. Moreover, this work has implications for experimental design in basic and translational research using human stem cell-derived retinal organoid models.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.