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Among all the organelles in an animal cell, only mitochondria have their own independent genomes. Animal mitochondrial DNA is a double-stranded, closed-circular molecule with around 20,000 base pairs. Mitochondrial DNA is unique in that one of its two strands, the heavy, or H, -strand is guanine rich, whereas the complementary strand is cytosine rich and called the light, or L, -strand. Compared to nuclear DNA, mitochondrial DNA has a very low percentage of non-coding regions and is marked by...
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Natural selection is an evolutionary process in which individuals with survival-promoting traits reproduce at higher rates. These favorable traits become more common within a population or species. Naturally selected traits initially arise via random genetic mutations. In order for selection to occur, there must be variation within a population, the trait controlling the variation must be heritable, and there must be an evolutionary advantage for variation in the trait.
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Mitochondrial dysfunction drives natural killer cell dysfunction in systemic lupus erythematosus.

Natalia W Fluder1, Morgane Humbel2, Emeline Recazens3

  • 1Department of Medicine, Division of Immunology and Allergy, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.

JCI Insight
|February 2, 2026
PubMed
Summary

Natural killer (NK) cells in systemic lupus erythematosus (SLE) show mitochondrial defects, impairing their function. Enhancing mitochondrial quality control with Urolithin A restored NK cell activity, suggesting a new therapeutic approach for SLE.

Keywords:
Autoimmune diseasesAutoimmunityImmunologyLupusNK cells

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Area of Science:

  • Immunology
  • Cell Biology
  • Mitochondrial Biology

Background:

  • Systemic lupus erythematosus (SLE) is an autoimmune disease with immune dysregulation.
  • Natural killer (NK) cells are functionally impaired in SLE, but mechanisms are unclear.

Purpose of the Study:

  • To investigate the role of mitochondrial dysfunction and mitophagy in SLE NK cell impairment.
  • To explore therapeutic strategies targeting mitochondrial quality control in SLE.

Main Methods:

  • Structural, metabolic, and proteomic analyses of SLE NK cells.
  • Transcriptional and proteomic profiling of mitophagy-related genes.
  • In vitro testing of mitophagy activators (Urolithin A) and Hydroxychloroquine.

Main Results:

  • SLE NK cells exhibit enlarged, dysfunctional mitochondria and impaired mitophagy.
  • Defective mitochondrial quality control correlates with reduced NK cell cytotoxicity and cytokine production.
  • Urolithin A restored mitochondrial function and NK cell responses; Hydroxychloroquine partially improved mitochondrial recycling.

Conclusions:

  • Impaired mitophagy and mitochondrial dysfunction are key contributors to NK cell defects in SLE.
  • Targeting mitochondrial quality control pathways may offer a novel therapeutic strategy for SLE.