ArticleScientific reports2026
Homovanillic acid improves anxiety by regulating F4/80+ microglia/macrophage in adult mice with neonatal cardiac injury.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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
Abstract
The heart-brain axis is a significant contributor to morbidity and mortality following ischemic injury. Pathological and psychological changes in the heart can lead to anxiety, cognitive impairment, and brain injury. Cardiac injury releases a substantial number of metabolites into the peripheral circulation, which exacerbates brain damage and dysfunction. Homovanillic acid (HVA), a metabolite of dopamine (DA), plays a crucial role in behavioral symptoms. However, there are limited studies examining the effects of cardiac metabolites released from an injured heart on behavioral symptoms in human juveniles, particularly in those who have suffered from severe cardiovascular diseases since childhood in human models. To study the potential role of injured cardiac metabolites on human juveniles’ behaviors, we use neonatal mouse heart cryoinjury to verify the mechanisms of heart-brain interactions in our study. Here, downregulated cardiac heart HVA is enriched in neonatal mouse injured heart at day 7 after injury, and meanwhile HVA treatment changes the physiology of the body such as heart weight/body weight, brain weight/body weight and thymus weight/body weight in mouse juveniles with chronic mouse cardiac injury. Additionally, HVA administration mediates anxiety-like behavior in the same group. Microglia/macrophages contribute to brain development and functions, potentially influencing on human behaviors, which is associates with MCP-1 expression. Mechanistically, we identifies the number of F4/80+ microglia/macrophage in adult mice with neonatal cardiac injury increases in HVA treatment, while there is no difference in mRNA and protein expression levels of MCP-1 at day 42 after injury. Thus, HVA may be a potential target in clinical behavioral symptoms with cardiovascular diseases.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.