Evidence map›Paper›PMID 40890617›Full record

ReviewBMC nephrology2025

Taming renal inflammation: signaling pathways and therapeutic advances in lupus nephritis.

Marsela Braunstein

Abstract readReview
In one paragraph

Review in BMC nephrology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
    Article
  3. Article
  4. Review
  5. Article
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

1 author.

Marsela Braunstein, Waterloo, ON, Canada. marsela.braunstein@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lupus nephritis (LN), a serious complication of systemic lupus erythematosus (SLE), involves complex immune dysregulation that leads to chronic renal inflammation and progressive tissue damage. Despite decades of use of standard immunosuppressive therapy, treatment responses remain variable, and many patients experience relapses or develop end-stage renal disease. This review synthesizes emerging insights into the immunopathogenesis of LN, drawing on studies from single-cell transcriptomics, signaling pathway analyses and renal tissue immunology. It examines the role of both innate and adaptive immune cells in mediating disease. The therapeutic landscape is rapidly evolving with novel biologics targeting B cell survival and cytokine signaling, small-molecule inhibitors modulating intracellular pathways, and promising developments in cell-based interventions. Notably, recent clinical case series have demonstrated that CD19-directed chimeric antigen receptor (CAR) T-cell therapy can induce durable drug-free remission in LN, representing a transformative approach to immune modulation. These advances are further supported by the application of multi-omics platforms to refine biomarker-driven disease monitoring and personalized treatment. Integrating immunologic and technological innovations holds the potential to redefine therapeutic strategies in LN. Precision medicine approaches that leverage targeted therapies, immune resetting modalities, and biomarker-guided clinical decisions may significantly improve long-term renal outcomes and patient quality of life.

Indexed as

Lupus NephritisSignal TransductionHumansImmunosuppressive AgentsImmunosuppressive AgentsImmune cellsLupus nephritisSignaling pathwaysTargeted therapy

Identifiers

PMID40890617
PMCPMC12400754

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.