ReviewCurrent rheumatology reports2024
The Role of Podocytes in Lupus Pathology.
Review in Current rheumatology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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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
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- SPARC upregulation mediates podocyte injury in Alport syndrome mice.BMC nephrology · 2026Article
- GBP2 promotes podocyte pyroptosis and contributes to the pathogenesis of pediatric lupus nephritis.PloS one · 2026Article
- CYBB-Mediated Ferroptosis Drives Podocyte Injury in Lupus Nephritis and Represents a Therapeutic Target.Journal of inflammation research · 2026Article
- The Pathogenesis, Potential Biomarkers and Novel Therapeutic Strategies for Tubulointerstitial Nephritis in Systemic Lupus Erythematosus-A Narrative Review.International journal of molecular sciences · 2025Review
- Podocyte, tubular epithelial-immune cell interplay in the pathogenesis of lupus nephritis.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purpose of reviewKidney injury due to lupus nephritis (LN) is a severe and sometimes life-threatening sequela of systemic lupus erythematosus. Autoimmune injury to podocytes has been increasingly demonstrated to be a key driver of LN-related kidney injury because these cells play key roles in glomerular filtration barrier homeostasis. Irreparable podocyte injury impairs these processes and can lead to proteinuria, which is an indicator of poor prognosis in LN. This review highlights recent advances in our understanding of the involvement of podocytes in the pathogenesis of LN and discusses new podocyte-targeted therapeutic strategies. RECENT
findingsPodocytes play a key role in glomerular filtration barrier homeostasis, both by helping to secrete and organize the glomerular basement membrane and by the formation of a glomerular slit diaphragm between adjacent cells. Recent studies revealed the involvement of abnormal calcium signaling, dysregulation of actin-related proteins, and mitotic catastrophe in LN progression. In addition, podocytes express many molecules related to the innate and adaptive immune responses. IgG from patients with LN induces direct injury of podocytes, inflammasome, and interactions with immune cells which have been shown to promote the development of LN. Our understanding of the role of podocytes in the pathogenesis of LN has been improved. Recent studies have shed light on potential therapeutic strategies targeting podocytes to control kidney injury.
Indexed as
Identifiers
39731699What 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.