Exploring cell-free mitochondria as a potential non-invasive biomarker of lupus nephritis

Authors

  • Khushboo Rana Babasaheb Bhimrao Ambedkar University, Lucknow India
  • Sharath Gowda Babasaheb Bhimrao Ambedkar University, Lucknow, India
  • Ankit Kumar Babasaheb Bhimrao Ambedkar University, Lucknow, India
  • Pradip Prajapati Babasaheb Bhimrao Ambedkar University, Lucknow, India
  • Namisha Patel Babasaheb Bhimrao Ambedkar University, Lucknow, India
  • Sapan Pandya Babasaheb Bhimrao Ambedkar University, Lucknow, India
  • Ratika Srivastava Babasaheb Bhimrao Ambedkar University, Lucknow, India

DOI:

https://doi.org/10.15305/ijir.v7i1.388

Abstract

Systemic lupus erythematosus (SLE) is a systemic chronic autoimmune disease. Lupus nephritis (LN) is one of the major manifestations of SLE affecting up to ~60% SLE patients. According to European League Against Rheumatism (EULAR) and American College of Rheumatology (ACR), a positive renal biopsy along with a positive antinuclear antibody (ANA) and/or anti-double-stranded DNA (anti-dsDNA) antibody is required for confirmation and classification of LN. Renal biopsy is the gold standard to diagnose and classify LN, but it is invasive and costly. Therefore, there is a need for less invasive, risk-free systemic biomarkers to predict disease activity and treatment outcomes. Cells under oxidative stress can release various mitochondrial Danger Associated Molecular Patterns (DAMPs) including naked or vesicle-enclosed forms of mitochondria itself known as cell-free mitochondria (cf-mitochondria), mitochondrial DNA etc. Stressful conditions are also well known to cause mitochondrial extrusion by damaged organs. The cf-mitochondria can act as auto-antigen, thus triggering immune response leading to production of anti-mitochondrial DNA autoantibodies.

Downloads

Published

17-11-2023

Issue

Vol. 7 No. 1 (2023)

Section

Abstracts

License

Copyright for articles published in this journal is retained by the authors, with first publication rights granted to the ‘Indian journal of Inflammation Research’. All the published content, except where otherwise noted, is licensed under Creative Commons license (CC-BY).

Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) after the publication of the manuscript in IJIR, as it can lead to productive exchanges, as well as earlier and greater citation of published work.