ArticleJournal of inflammation research2024
Overproduction of Mitochondrial Fission Proteins and Mitochondrial Fission in Podocytes of Lupus Nephritis Patients.
Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Identification and functional characterisation of SCO1 as a mitochondria-related biomarker in lupus nephritis.Lupus science & medicine · 2026Article
- Mitochondrial morphological aberrations and redistribution in podocytes with glomerular diseases.Renal failure · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: The glomerular injury is associated with different pathogeneses, and podocyte damage is common in various ISN/RPS class lupus nephritis (LN). In podocyte, mitochondrial morphological changes are observed in lupus nephritis (LN) in our previous study. This study aimed to explore mitochondrial fission proteins expression in podocytes using bioinformatics analysis and further to investigate the associations between mitochondrial fission proteins and laboratory features in LN. Methods: To determine the differentially expressed genes (DEGs) between LN and normal controls, we downloaded and analyzed microarray datasets. Then download the mitochondrial genes list from the MitoMiner 4.0 database, then take the genes that are common with the DEGs. Functional enrichment analyses were then performed. Then mitochondrial fission was observed through electron microscope. We performed immunofluorescence staining to explore the expression of mitochondrial fission proteins in LN patients. Results: Among these 658 DEGs, 5 DEGs related to mitochondrial dynamics were identified. Mitochondrial dynamics proteins were involved in mitophagy. Mitochondrial fission proteins Drp1 and Fis1 staining were significantly enhanced compared to that in the controls. 24h-UTP are positively correlated with mitochondrial fission proteins expression. Conclusion: Mitochondrial fission was observed in LN patients' podocytes. Mitochondrial fission proteins Drp1 and Fis1 were overproduced in podocytes, and then they can lead to mitochondrial fission, which may aggravate podocyte damage and proteinuria. While the mechanism still needs to be explored.
Indexed as
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.