Evidence map›Paper›PMID 32117292›Full record

ArticleFrontiers in immunology2020

A Systematic Investigation on Complement Pathway Activation in Diabetic Retinopathy.

Shahna Shahulhameed, Sushma Vishwakarma, Jay Chhablani, Mudit Tyagi, Rajeev R Pappuru, Saumya Jakati, Subhabrata Chakrabarti, Inderjeet Kaur

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
8.6field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

61 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Neuroinflammation in glaucoma: a myriad of cellular pathways and players.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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  14. Neuritin 1 Drives Therapeutic Preservation of Retinal Ganglion Cells in anJournal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2024
    Article
  15. Modulation of diabetes-related retinal pathophysiology by PTX3.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article

1 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Shahna ShahulhameedProf Brien Holden Eye Research Centre, LV Prasad Eye Institute, Hyderabad, India.
Sushma VishwakarmaProf Brien Holden Eye Research Centre, LV Prasad Eye Institute, Hyderabad, India.
Jay ChhablaniSmt. Kanuri Santhamma Center for Vitreo Retinal Diseases, LV Prasad Eye Institute, Hyderabad, India.
Mudit TyagiSmt. Kanuri Santhamma Center for Vitreo Retinal Diseases, LV Prasad Eye Institute, Hyderabad, India.
Rajeev R PappuruMedical Retina and Vitreoretinal Surgery, University of Pittsburgh School of Medicine, Pittsburgh, PA, United States.
Saumya JakatiOphthalmic Pathology Laboratory, LV Prasad Eye Institute, Hyderabad, India.
Subhabrata ChakrabartiProf Brien Holden Eye Research Centre, LV Prasad Eye Institute, Hyderabad, India.
Inderjeet KaurProf Brien Holden Eye Research Centre, LV Prasad Eye Institute, Hyderabad, India.
L V Prasad Eye Institute · INUniversity of Pittsburgh · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The complement system plays a crucial role in retinal homeostasis. While the proteomic analysis of ocular tissues in diabetic retinopathy (DR) has shown the deposition of complement proteins, their exact role in the pathogenesis of DR is yet unclear. We performed a detailed investigation of the role of the complement system by evaluating the levels of major complement proteins including C3, C1q, C4b, Complement Factor B (CFB), and Complement Factor H (CFH) and their activated fragments from both the classical and alternative pathways in vitreous humor and serum samples from proliferative DR (PDR) patients and controls. Further, the expressions of complements and several other key pro- and anti-angiogenic genes in the serum and vitreous humor were analyzed in the blood samples of PDR and non-PDR (NPDR) patients along with controls without diabetes. We also assessed the pro-inflammatory cytokines and matrix metalloproteinases in the vitreous humor samples. There was a significant increase in C3 and its activated fragment C3bα' (110 kDa) along with a corresponding upregulation of CFH in the vitreous of PDR patients, which confirmed the increased activation of the alternative complement pathway in PDR. Likewise, a significant upregulation of angiogenic genes and downregulation of anti-angiogenic genes was seen in PDR and NPDR cases. Increased MMP9 activity and upregulation of inflammatory markers IL8 and sPECAM with a downregulation of anti-inflammatory marker IL-10 in PDR vitreous indicated the possible involvement of microglia in DR pathogenesis. Further, a significantly high C3 deposition in the capillary wall along with thickening of basement membranes and co-localization of CFH expression with CD11b

Indexed as

Complement Pathway, AlternativeComplement Pathway, ClassicalAgedBiomarkersCase-Control StudiesComplement C3Complement Factor HCytokinesDiabetic RetinopathyFemaleHumansMaleMicrogliaMiddle AgedNeovascularization, PathologicRetinaBiomarkersComplement C3Complement Factor HCytokinesangiogenesiscomplement pathwaydiabetic retinopathyinflammationmicrogliaretinavitreous humor

Identifiers

PMID32117292
PMCPMC7026189
OpenAlexW3006264708

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.