ArticleJournal of inflammation research2021
CTRP9 Enhances Efferocytosis in Macrophages via MAPK/Drp1-Mediated Mitochondrial Fission and AdipoR1-Induced Immunometabolism.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Efferocytosis: the art of cellular clearance and novel perspectives in disease therapy.Molecular cancer · 2025Review
- Analysis of the Mitochondrial Dynamics in NAFLD: Drp1 as a Marker of Inflammation and Fibrosis.International journal of molecular sciences · 2025Article
- Functional transformation of macrophage mitochondria in cardiovascular diseases.Molecular and cellular biochemistry · 2025Review
- The Potential Role of Cardiokines in Heart and Kidney Diseases.Current medicinal chemistry · 2025Review
- Mesenchymal stem cell-derived extracellular vesicles relieve endothelial cell senescence via recovering CTRP9 upon repressing miR-674-5p in atherosclerosis.Regenerative therapy · 2024Article
- SIRT3 Regulates Clearance of Apoptotic Cardiomyocytes by Deacetylating Frataxin.Circulation research · 2023Article
- Ubiquitin-specific protease 11-mediated CD36 deubiquitination acts on C1q/TNF-related protein 9 against atherosclerosis.ESC heart failure · 2023Article
- Expression of Serum Omentin, CTRP9, and Vaspin in Patients with Polycystic Ovary Syndrome.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Insights Into Mitochondrial Dynamics in Chlamydial Infection.Frontiers in cellular and infection microbiology · 2022Review
- Prohibitins: A Key Link between Mitochondria and Nervous System Diseases.Oxidative medicine and cellular longevity · 2022Review
- The Role of Anti-Inflammatory Adipokines in Cardiometabolic Disorders: Moving beyond Adiponectin.International journal of molecular sciences · 2021Review
- Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundClearance of apoptotic cells (ACs) by phagocytes (efferocytosis) suppresses post-apoptotic necrosis and alleviates inflammation. Defective efferocytosis induces diseases that include atherosclerosis and autoimmune diseases. C1q/TNF-related protein 9 (CTRP9), a novel adipokine, has been reported to protect against various cardiovascular disease; however, the effect of CTRP9 on efferocytosis has not been elucidated.
methods1. The efferocytosis of macrophages incubated with ACs with or without CTRP9 treatment was detected by flow cytometry (FCM) and immunostaining. The unengulfed ACs of CTRP9-KO and wild-type (WT) mice after dexamethasone injection were detected by TUNEL assay. 2. As mitochondrial fission is important for promoting efferocytosis, the effect of CTRP9 on mitochondrial fission was measured by fission/fusion-related proteins (MFN2, DRP1, MFF, and OPA1) and visualized by staining with MitoTracker. 3. On account of metabolism insults in engulfed macrophages, we conducted a two-stage efferocytosis assay, and the protective effects of CTRP9 on metabolism were investigated by Western blot.
resultsCTRP9 significantly facilitated macrophage efferocytosis, and it promoted mitochondrial fission by increasing the expression of p-DRP1 (s616) and the translocation of DRP1 from the cytoplasm to the mitochondria. The p38/Jnk-MAPK pathway was activated after treatment with 1 μg/mL CTRP9. When we blocked the activation of MAPK signaling by SB203580 and SP600125, the mediated effect on p-DRP1 (s616) was reduced. Moreover, CTRP9 increased the levels of ABCA1, PPAR-y, HIF-1a and GLUT1, as well as the release of lactate in basal and engulfed macrophages, which revealed that the metabolism of macrophages was advanced. Apoptotic cell-conditioned media (ACCM) and ACs increased the expression of adiponectin receptor 1 (AdipoR1). Down-regulation of AdipoR1 by siRNA could abrogate the immunometabolism effects of CTRP9.
conclusionCTRP9 promoted efferocytosis in macrophages via MAPK/drp1-mediated mitochondrial fission and AdipoR1-induced immunometabolism.
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