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Molecular Mechanisms Associated to Systemic Lupus Erythematosus

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 2828

Special Issue Editor


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Guest Editor
Cardiometabolic and Renal Risk Research Group, INCLIVA Biomedical Research Institute, Avd. Menendez Pelayo, accesorio 4, 46010 Valencia, Spain
Interests: drug delivery systems; non-coding RNA; extracellular vesicles; exosomes; blood-urine-renal delivery; renal glomerular crosstalk; translational research
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Special Issue Information

Dear Colleagues,

Systemic lupus erythematosus (SLE) is a complex multisystem autoimmune disease extremely heterogeneous with a wide spectrum of different combinations of clinical manifestations, accumulation of laboratory and immunological abnormalities, and a variable disease progression and outcome. The etiology and pathogenesis of SLE are accompanied by immune disorders including abnormal activation, proliferation, differentiation, and dysfunction of immune cells. Over-secretion of autoantibodies against several cellular compartments triggers cytokine production by innate immune cells and incite tissue and organ inflammation. Despite considerable progress regarding the knowledge of the SLE pathophysiology, patients suffer a deficient and late diagnosis that conditions the disease progression. Determining a SLE patient-tailored preventive strategy remains a crucial problem to be resolved. This special issue welcomes original research manuscripts investigating novel molecular biomarkers that regulate critical pathways in SLE-associated activity and renal damage progression, the most common and serious manifestation in SLE, or new molecular regulatory networks identified by biology system analysis; critical reviews that summarize recent advances in this field and provide a rationale for further research are also welcome.

Dr. Raquel Cortes Vergaz
Guest Editor

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Keywords

  • systemic lupus erythematosus
  • lupus nephritis
  • molecular mechanisms
  • next generation sequencing
  • immune cells
  • extracellular vesicles
  • non-coding RNA
  • biology system analysis

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Published Papers (1 paper)

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Research

15 pages, 3278 KiB  
Article
Plasma Exosomal Non-Coding RNA Profile Associated with Renal Damage Reveals Potential Therapeutic Targets in Lupus Nephritis
by Ana Flores-Chova, Olga Martinez-Arroyo, Angela L. Riffo-Campos, Ana Ortega, Maria J. Forner and Raquel Cortes
Int. J. Mol. Sci. 2023, 24(8), 7088; https://doi.org/10.3390/ijms24087088 - 11 Apr 2023
Cited by 7 | Viewed by 2463
Abstract
Despite considerable progress in our understanding of systemic lupus erythematosus (SLE) pathophysiology, patient diagnosis is often deficient and late, and this has an impact on disease progression. The aim of this study was to analyze non-coding RNA (ncRNA) packaged into exosomes by next-generation [...] Read more.
Despite considerable progress in our understanding of systemic lupus erythematosus (SLE) pathophysiology, patient diagnosis is often deficient and late, and this has an impact on disease progression. The aim of this study was to analyze non-coding RNA (ncRNA) packaged into exosomes by next-generation sequencing to assess the molecular profile associated with renal damage, one of the most serious complications of SLE, to identify new potential targets to improve disease diagnosis and management using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. The plasma exosomes had a specific ncRNA profile associated with lupus nephritis (LN). The three ncRNA types with the highest number of differentially expressed transcripts were microRNAs (miRNAs), long non-coding RNAs (lncRNAs) and piwi-interacting RNAs (piRNAs). We identified an exosomal 29-ncRNA molecular signature, of which 15 were associated only with LN presence; piRNAs were the most representative, followed by lncRNAs and miRNAs. The transcriptional regulatory network showed a significant role for four lncRNAs (LINC01015, LINC01986, AC087257.1 and AC022596.1) and two miRNAs (miR-16-5p and miR-101-3p) in network organization, targeting critical pathways implicated in inflammation, fibrosis, epithelial–mesenchymal transition and actin cytoskeleton. From these, a handful of potential targets, such as transforming growth factor-β (TGF-β) superfamily binding proteins (activin-A, TGFB receptors, etc.), WNT/β-catenin and fibroblast growth factors (FGFs) have been identified for use as therapeutic targets of renal damage in SLE. Full article
(This article belongs to the Special Issue Molecular Mechanisms Associated to Systemic Lupus Erythematosus)
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