ArticleNature communications2025
Reprogramming mitochondrial metabolism and epigenetics of macrophages via miR-10a liposomes for atherosclerosis therapy.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed.
- Revisiting Alzheimer's Disease Through the Somatostatin-Mitochondria Axis.Molecular neurobiology · 2026Review
- Cell-Surface Signatures and Targets of Modulated Vascular Smooth Muscle Cells in Atherosclerosis: From State Identification to Precision Intervention.Journal of cardiovascular development and disease · 2026Review
- Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026Review
- Application of nanotherapy in cardiovascular diseases featuring novel pharmacological mechanisms and drug delivery strategies.Discover nano · 2026Review
- A Cathepsin-Triggered Size-Shrinkable Nanoparticle Enhances Fibrous Cap Penetration to Relieve Atherosclerosis.Advanced healthcare materials · 2026Article
- Functional Heterogeneity of Immune Cell Subpopulations in Atherosclerosis: From Basic Mechanisms to Precision Therapy.Reviews in cardiovascular medicine · 2026Review
- MicroRNAs as master regulators of macrophage function in atherosclerosis: From polarization to therapeutic potential.iScience · 2026Review
- Fatty Acid Metabolism in Health and Cancer: From Fundamental Mechanisms to Therapeutic Application.MedComm · 2026Review
- Regulation of mitochondrial biogenesis and energy metabolism in the heart.Chinese medical journal · 2026Review
- Mitochondrial respiration and nucleotide profiling in human left internal mammary artery from CABG: a novel real-timeActa biochimica Polonica · 2026Article
- Natural polysaccharides as immunometabolic modulators in metabolic diseases: mechanisms and translational challenges.Frontiers in immunology · 2026Review
- From support to homeostatic licensing: the bidirectional fibroblast-macrophage circuit and its central role in tissue homeostasis and fibrosis.Frontiers in immunology · 2026Review
- Plasma-derived mitochondria as a minimal manipulation alternative for attenuating inflammatory immune responses.Regenerative biomaterials · 2026Article
- Bibliometric analysis of research hotspots and emerging trends in microRNAs and atherosclerosis (2007-2025).Frontiers in cardiovascular medicine · 2026Review
- A mitochondrial-stress adipocyte-macrophage circuit sustaining metaflammation in human type 2 diabetic adipose tissue.Frontiers in immunology · 2026Article
- Mitochondria-targeted nanotechnology in cardiovascular diseases: a review of recent advances.Regenerative biomaterials · 2026Review
- Nanoparticles Used for the Delivery of RNAi-Based Therapeutics.Pharmaceutics · 2025Review
- Epigenetic modifications in vascular inflammation.Frontiers in immunology · 2025Review
- Decoding cardiac metabolic reprogramming through single-cell multi-omics: from mechanisms to therapeutic applications.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Disruption in the dynamic stability of macrophage pro/anti-inflammatory phenotypes within plaques significantly impacts chronic vascular inflammation and exacerbates atherosclerosis. Reprogramming macrophages from pro-inflammatory to anti-inflammatory phenotype mitigates atherosclerosis progression. However, chronic inflammatory stimulation induces a closed chromatin state in atherosclerotic macrophages, inhibiting their phenotype reprogramming. This study demonstrates that restoring mitochondrial respiration increases histone acetylation (AcH3) and enhances chromatin accessibility in atherosclerotic macrophages, restarting macrophage phenotype reprogramming. Additionally, we identified that miR-10a can facilitate mitochondrial respiration and reorganize macrophage reprogramming. To optimize delivery, prolong circulation time, and target pro-inflammatory macrophages, we developed red blood cell membrane-modified liposome nanoparticles (miR-10a@H-MNP) to deliver miR-10a. Hyaluronic acid was conjugated to the liposomes to specifically target pro-inflammatory macrophages in plaque. Intravenous administration of miR-10a@H-MNP significantly alleviated atherosclerosis progression in male mice. Thus, the epigenomic priming approach developed here effectively triggers macrophage reprogramming in atherosclerosis, presenting a promising metabolically based epigenetic modulation method for plaque clearance.
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What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.