94% of researchers rate our articles as excellent or good
Learn more about the work of our research integrity team to safeguard the quality of each article we publish.
Find out more
Makoto Ishikawa1,2*
Yukitoshi Izumi3,4,5
Kota Sato1,6
Taimu Sato1
Charles F. Zorumski3,4,5Hiroshi Kunikata1,7Toru Nakazawa1,2,6,7- 1Department of Ophthalmology, Tohoku University Graduate School of Medicine, Sendai, Japan
- 2Department of Ophthalmic Imaging and Information Analytics, Tohoku University Graduate School of Medicine, Sendai, Japan
- 3Taylor Family Institute for Innovative Psychiatric Research, Washington University School of Medicine, St. Louis, MO, United States
- 4Center for Brain Research in Mood Disorders, Washington University School of Medicine, St. Louis, MO, United States
- 5Department of Psychiatry, Washington University School of Medicine, St. Louis, MO, United States
- 6Department of Advanced Ophthalmic Medicine, Tohoku University Graduate School of Medicine, Sendai, Japan
- 7Department of Retinal Disease Control, Tohoku University Graduate School of Medicine, Sendai, Japan
A Corrigendum on
Glaucoma and microglia-induced neuroinflammation
by Ishikawa M, Izumi Y, Sato K, Sato T, Zorumski CF, Kunikata H and Nakazawa T (2023) Front. Ophthalmol. 3:1132011. doi: 10.3389/fopht.2023.1132011
Incorrect Reference
In the published article, one of the references has been retracted. This article has been removed, and replaced with the following article: Tremblay MÈ, Stevens B, Sierra A, Wake H, Bessis A, Nimmerjahn A. The role of microglia in the healthy brain. J Neurosci (2011) 31(45):16064-9. doi: 10.1523/JNEUROSCI.4158-11.2011
The article text has also been updated to reflect this change. The first paragraph of Section 2, Functions of Microglia in the Retina, previously read as follows:
“Microglia are thought to derive from monocytes that enter the retina from the blood stream during development, and dynamically move their cellular projections even under physiological conditions (12), making physical contact with neurons and synapses and performing synaptic pruning to remove unnecessary synapses. In the development of excitatory circuits, synaptic pruning, by which extrasynaptic connections are eliminated by microglia, is thought to occur when complement C1q is expressed at synapses by TGF-β secreted from astrocytes (13).”
The corrected sentence appears below:
“Microglia are thought to derive from monocytes that enter the retina from the blood stream during development, and dynamically move their cellular projections even under physiological conditions (12), making physical contact with neurons and synapses and performing synaptic pruning to remove unnecessary synapses (13).”
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
Publisher’s note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
Keywords: glaucoma, neuroinflammation, microglia, NOD-like receptor pyrin domain containing 3 inflammasome, retinal ganglion cell damage
Citation: Ishikawa M, Izumi Y, Sato K, Sato T, Zorumski CF, Kunikata H and Nakazawa T (2023) Corrigendum: Glaucoma and microglia-induced neuroinflammation. Front. Ophthalmol. 3:1332312. doi: 10.3389/fopht.2023.1332312
Received: 02 November 2023; Accepted: 09 November 2023;
Published: 01 December 2023.
Edited and Reviewed by:
Youichi Shinozaki, Tokyo Metropolitan Institute of Medical Science, JapanCopyright © 2023 Ishikawa, Izumi, Sato, Sato, Zorumski, Kunikata and Nakazawa. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Makoto Ishikawa, bWFrb3RvLmlzaGlrYXdhLmMyQHRvaG9rdS5hYy5qcA==