ReviewIrish journal of medical science2025
BDNF-TrkB signalling: a neurotrophic pathway to cardiovascular protection.
Review in Irish journal of medical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Neurotrophin System Alterations Associated with Neurotoxicity Accompanied by Carotid Artery Diseases-A Systematic Review.International journal of molecular sciences · 2026Pooled it
- Effects ofPreventive nutrition and food science · 2026Article
- Association between atherogenic dyslipidemia and DBS-derived p-tau217 in older adults: evidence from SHARE DBS data.Frontiers in aging neuroscience · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase B (TrkB) signaling axis has emerged as a promising frontier in cardiovascular research, particularly in the context of myocardial ischemia/reperfusion (I/R) injury. Originally recognized for its neuroprotective functions, BDNF is now gaining recognition for its cardioprotective properties, including anti-apoptotic effects, improved cardiomyocyte survival, and enhanced contractile function. Acting predominantly through TrkB, BDNF attenuates ischemia-induced apoptosis by downregulating caspase-3 and cleaved caspase-9, while simultaneously promoting cardiomyocyte differentiation and proliferation. Intriguingly, under hypoxic conditions, a shift from p75NTR to TrkB receptor activity amplifies these protective effects. Moreover, BDNF modulates intracellular calcium handling by activating Ca
Indexed as
Identifiers
40668524What 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.