ReviewJournal of molecular and cellular cardiology2011
Nix Nought Nothing: fairy tale or real deal.
Review in Journal of molecular and cellular cardiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 16 citations in OpenAlex.
- Myocardin regulates mitochondrial calcium homeostasis and prevents permeability transition.Cell death and differentiation · 2018Article
- Autophagy as an emerging target in cardiorenal metabolic disease: From pathophysiology to management.Pharmacology & therapeutics · 2018Review
- The fibrosis-cell death axis in heart failure.Heart failure reviews · 2016Review
- Article
- Epigenetic regulation of E2F-1-dependent Bnip3 transcription and cell death by nuclear factor-κB and histone deacetylase-1.Pediatric cardiology · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Nix was first described in the heart as the protein product of a differentially expressed mRNA detected by hybridization to a partial cDNA sequence tag on an RNA expression array. Over the subsequent 8 years Nix has become the prototypical transcriptionally-regulated cardiac myocyte "suicide" gene and has been used as a model to interrogate mechanisms of programmed cardiomyocyte death in hypertrophy and heart failure. Nix stimulates conventional apoptosis mediated via the intrinsic mitochondrial pathway, but emerging evidence indicates that Nix also controls programmed necrosis dependent upon sarcoplasmic reticular-mitochondrial tethering, calcium cross-talk, and the mitochondrial permeability transition. Recent studies have also described Nix labeling of senescent cardiomyocyte mitochondria for autophagic elimination, elucidated a physiological mitochondrial quality control Nix function; so-called "mitochondrial pruning". This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure."
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.