ArticleMaterials today. Bio2025
A tripartite therapeutic agent reprograms the myocardial infarction microenvironment.
Article in Materials today. Bio, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- SIRT3 in post-myocardial infarction macrophage reprogramming: linking mitochondrial fitness to inflammation resolution and repair.Frontiers in immunology · 2026Pooled it
- The Application of Injectable Hydrogels in Myocardial Infarction Repair: Material Design, Biological Functions and Clinical Translation.International journal of molecular sciences · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction (MI) remains a global health challenge despite advances in reperfusion therapies, as subsequent oxidative stress, inflammatory cascades, and electrical conduction abnormalities impede functional recovery. This study presents a tripartite therapeutic strategy addressing these pathological mechanisms through a clinically translatable multifunctional myocardial repair agent (MMRA). The system combines polypyrrole's and sinomenine's (Sino) anti-inflammatory/antioxidant effects, formulated within a conductive thermoresponsive Poloxamer 407 (P407) hydrogel platform. Injectable P407 hydrogel facilitates targeted delivery and sustained release of therapeutic components within the infarct zone. In vivo evaluations revealed MMRA's capacity to simultaneously: 1) Scavenge reactive oxygen species and downregulate pro-inflammatory cytokines, 2) Reprogram macrophage polarization toward tissue-reparative M2 phenotypes and 3) Restore electrical signal propagation through conductive hydrogel-mediated intercellular coupling. By synergistically modulating the post-infarction microenvironment while preserving myocardial electromechanical synchronization, this integrated therapeutic paradigm demonstrates significant potential for enhancing cardiac repair outcomes. The employment of clinically approved components (Sino and P407) further shows the excellent translational feasibility of the MMRA for MI treatment.
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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.