ArticleCirculation research2012
Inflame on!: mitochondrial escape provokes cytokine storms that doom the heart.
Article in Circulation research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 6 citations in OpenAlex.
- Cytokine storm in acute respiratory distress syndrome.Journal of intensive medicine · 2026Review
- Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025Review
- Fulminant myocarditis: a comprehensive review from etiology to treatments and outcomes.Signal transduction and targeted therapy · 2020Review
- Picking up a Fight: Fine Tuning Mitochondrial Innate Immune Defenses Against RNA Viruses.Frontiers in microbiology · 2020Review
Corrections and comments
- Comment on
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are derived from primordial bacterial endosymbionts and retain partial genomes. In mammalian cells, damaged or dysfunctional mitochondria are recognized, targeted for elimination, then neatly packaged and eliminated via mitophagy. A recent paper from Oka et al describes how interrupting normal mitophagic mitochondrial DNA degradation after pressure overload can activate Toll-like receptor-9 mediated innate immunity, causing myocardial inflammation that contributes to cardiomyopathic decompensation.
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.