ReviewJournal of inflammation research2026
ATP-P2X7R-NLRP3 Axis as a Unifying Mechanism of ATP-Induced Cell Death in Degenerative Bone and Cardiovascular Diseases.
Review in Journal of inflammation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
- S100A9 as a shared biomarker and mediator of metabolic dysfunction in peripheral artery disease and sarcopenia.Frontiers in genetics · 2026Article
- Microbiota-innate immune crosstalk drives atherosclerosis: mechanisms, disease progression, and emerging therapeutic strategies.Frontiers in immunology · 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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extracellular Adenosine triphosphate (ATP), acting as both an energy signal and damage-associated molecular pattern (DAMP), plays a critical role in the progression of degenerative bone diseases (DBD) and cardiovascular diseases (CVD). Through activation of purinergic receptors, particularly P2X7, ATP induces a cascade of events leading to ATP-induced cell death (AICD), characterized by calcium influx, mitochondrial dysfunction, oxidative stress, and inflammasome activation, culminating in pyroptosis, apoptosis, and ferroptosis. These processes are implicated in osteoarthritis (OA), intervertebral disc degeneration (IVDD), osteoporosis (OP), and cardiovascular conditions such as myocardial infarction and heart failure. The ATP-P2X7-NLRP3 axis emerges as a shared molecular mechanism linking these diseases, driven by energy imbalance and chronic inflammation. This review explores the molecular mechanisms of AICD in DBD and CVD, evaluates experimental and clinical evidence, and discusses potential therapeutic strategies targeting the ATP-purinergic-mitochondrial axis, offering insights into integrated treatment approaches for both disease types.
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Identifiers
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.