ArticleKidney international2022
Conditional deletion of myeloid-specific mitofusin 2 but not mitofusin 1 promotes kidney fibrosis.
Article in Kidney international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 37 citations in OpenAlex.
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- Adipose Mesenchymal Stem Cells Secreted Exosomal miR-26a-5p Ameliorate Renal Fibrosis via Inhibiting Glycolysis and Ferroptosis in Renal Interstitial Fibrosis.Journal of cellular and molecular medicine · 2026Article
- Identification of biomarkers associated with mitochondria and macrophage polarization in acute myocardial infarction: a bioinformatics analysis and validation study.Journal of cardiothoracic surgery · 2026Article
- Mitophagy and Cellular Homeostasis in Kidney Diseases: Mechanisms and Potential Therapeutics.International journal of biological sciences · 2026Review
- The plasticity and metabolic reprogramming of macrophage in ulcerative colitis.Frontiers in immunology · 2026Review
- Mitochondrial dysfunction: the hidden catalyst in chronic kidney disease progression.Renal failure · 2025Review
- CAMKK2 restored mitochondrial dynamics homeostasis to alleviate pulmonary fibrosis via AMPK/PGC-1α signaling pathway in lung fibroblasts.Molecular medicine (Cambridge, Mass.) · 2025Article
- Mitochondria-driven inflammation: a new frontier in ovarian ageing.Journal of translational medicine · 2025Review
- Therapeutic restoration of mitochondria-endoplasmic reticulum cross talk for osteoarthritis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Targeting mitochondrial dysfunction: an innovative strategy for treating renal fibrosis.Molecular and cellular biochemistry · 2025Review
- The Role of mtDNA Mutations in Atherosclerosis: The Influence of Mitochondrial Dysfunction on Macrophage Polarization.International journal of molecular sciences · 2025Review
- Autophagy and Mitophagy in Diabetic Kidney Disease-A Literature Review.International journal of molecular sciences · 2025Review
- The multifaceted role of macrophages in kidney physiology and diseases.Frontiers in immunology · 2025Review
- Editorial: Diabetic kidney disease: routes to drug development, pharmacology and underlying molecular mechanisms, volume II.Frontiers in pharmacology · 2025Article
- Mitophagy Regulates Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2024Review
- The interactions of subcellular organelles in pulmonary fibrosis induced by carbon black nanoparticles: a comprehensive review.Archives of toxicology · 2024Review
- Profibrogenic macrophage-targeted delivery of mitochondrial protector via exosome formula for alleviating pulmonary fibrosis.Bioactive materials · 2024Article
- Mitophagy in fibrotic diseases: molecular mechanisms and therapeutic applications.Frontiers in physiology · 2024Review
- Macrophage polarization and its impact on idiopathic pulmonary fibrosis.Frontiers in immunology · 2024Review
- Mitophagy in renal interstitial fibrosis.International urology and nephrology · 2024Review
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Authors and funding
7 authors at 1 institution in 2 countries.
Funding
Abstract
Macrophages exert critical functions during kidney injury, inflammation, and tissue repair or fibrosis. Mitochondrial structural and functional aberrations due to an imbalance in mitochondrial fusion/fission processes are implicated in the pathogenesis of chronic kidney disease. Therefore, we investigated macrophage-specific functions of mitochondrial fusion proteins, mitofusin (MFN)1 and MFN2, in modulating macrophage mitochondrial dynamics, biogenesis, oxidative stress, polarization, and fibrotic response. MFN1 and MFN2 were found to be suppressed in mice after adenine diet-induced chronic kidney disease, in transforming growth factor-beta 1-treated bone marrow-derived macrophages, and in THP-1-derived human macrophages (a human leukemic cell line). However, abrogating Mfn2 but not Mfn1 in myeloid-lineage cells resulted in greater macrophage recruitment into the kidney during fibrosis and the macrophage-derived fibrotic response associated with collagen deposition culminating in worsening kidney function. Myeloid-specific Mfn1 /Mfn2 double knockout mice also showed increased adenine-induced fibrosis. Mfn2-deficient bone marrow-derived macrophages displayed enhanced polarization towards the profibrotic/M2 phenotype and impaired mitochondrial biogenesis. Macrophages in the kidney of Mfn2-deficient and double knockout but not Mfn1-deficient mice exhibited greater mitochondrial mass, size, oxidative stress and lower mitophagy under fibrotic conditions than the macrophages in the kidney of wild-type mice. Thus, downregulation of MFN2 but not MFN1 lead to macrophage polarization towards a profibrotic phenotype to promote kidney fibrosis through a mechanism involving suppression of macrophage mitophagy and dysfunctional mitochondrial dynamics.
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Registered trials
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