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Mertk-driven tunneling nanotube formation in macrophages preserves mitochondrial homeostasis during kidney

Jun Zeng1, Ruoqing Li2, Liyin Chai1

  • 1Department of Nephrology, Chongqing Key Laboratory of Emergency Medicine, Chongqing Emergency Medical Center, Chongqing University Central Hospital, School of Medicine, Chongqing University, Chongqing, China.

Biochemical Pharmacology
|January 16, 2026
PubMed

Insights

Mertk deficiency worsens kidney injury by impairing mitochondrial function. Mertk-expressing macrophages protect kidney cells via tunneling nanotubes, transferring mitochondria and offering a therapeutic target for acute kidney injury.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Renal ischemia-reperfusion (I/R) injury is a major cause of acute kidney injury (AKI) and organ transplant complications.
  • This injury involves oxidative stress, inflammation, and mitochondrial dysfunction.
  • The role of Mertk, a macrophage-expressed protein, in renal I/R injury is not well understood.

Purpose of the Study:

  • To investigate the role of Mertk in renal I/R injury.
  • To elucidate the mechanisms by which Mertk influences kidney-resident macrophages (KRMs) and renal tubular epithelial cells (RTECs) during I/R injury.

Main Methods:

  • Utilized Mertk knockout (Mertk-KO) and wild-type (WT) mice subjected to renal I/R injury.
  • Performed in vitro studies involving Mertk knockdown and overexpression in KRMs under hypoxia-reoxygenation (H/R).
  • Assessed tubular injury, inflammation, oxidative stress, mitochondrial function, and tunneling nanotubes (TNTs) formation.

Main Results:

  • Mertk deficiency exacerbated renal tubular injury, inflammation, and oxidative stress in I/R-induced AKI.
  • Mertk deficiency led to decreased ATP production and disrupted mitochondrial morphology in RTECs.
  • Mertk overexpression in KRMs attenuated H/R-induced injury, promoting TNTs formation and intercellular mitochondrial transfer to RTECs.

Conclusions:

  • Mertk plays a protective role in renal I/R injury by mediating crosstalk between KRMs and RTECs.
  • Mertk facilitates mitochondrial homeostasis in RTECs through TNT-dependent mitochondrial transfer from KRMs.
  • Targeting Mertk-mediated mitochondrial transfer via TNTs presents a potential therapeutic strategy for AKI.
Keywords:
Acute kidney injuryIschemia–reperfusionKidney-resident macrophagesMertkMitochondrial homeostasisTunneling nanotubes

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