ReviewRegenerative biomaterials2026
Mitochondria-targeted nanotechnology in cardiovascular diseases: a review of recent advances.
Review in Regenerative biomaterials, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular diseases (CVDs) remain the leading cause of global mortality, with mitochondrial dysfunction serving as a central pathological hub in conditions such as atherosclerosis, myocardial ischemia-reperfusion injury and heart failure. Current mitochondrial-regulating drugs are severely limited by low bioavailability, short duration of action, poor targeting specificity and off-target effects, highlighting an urgent need for precise delivery systems. Nanocarriers, with tunable physicochemical properties and surface functionalization potential, enable hierarchical targeting of diseased cardiac tissues and mitochondria, offering a novel solution to overcome these limitations. Preclinical models have shown promising efficacy, particularly in alleviating oxidative stress damage in ischemic cardiomyopathy, improving energy metabolism in heart failure and promoting tissue repair. These encouraging results have sparked growing interest in the application of nanomaterials for mitochondrial-targeted diagnosis and treatment of CVDs. This review first outlines the role of mitochondrial dysfunction in CVD pathogenesis, covering impaired oxidative phosphorylation, excessive reactive oxygen species production, disrupted mitochondrial dynamics and defective mitophagy. It, then, focuses on the design strategies of nanotherapeutics based on a hierarchical targeting concept, encompassing the selection of biocompatible carriers, optimization of size and morphology, tissue or cell-specific targeting modifications, mitochondrial ligand modifications, as well as the loading and therapeutic mechanisms of various therapeutic agents. Furthermore, it provides an in-depth analysis of key physiological barriers such as hemodynamic shear stress, endothelial barrier and extracellular matrix hindrance, along with intracellular trafficking challenges including lysosomal escape and immune clearance, which all impact delivery efficiency. This review aims to offer insights to advance the rational development and clinical translation of mitochondria-targeted nanomedicines for CVDs.
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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.