ReviewFrontiers in immunology2016
Cytochrome c as a Potentially Clinical Useful Marker of Mitochondrial and Cellular Damage.
Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers, 1 of them a synthesis that pooled it.
What it found
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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
97 citing papers in PubMed, 1 synthesis or guideline pooled it, 204 citations in OpenAlex.
- Programmed cell death detection methods: a systematic review and a categorical comparison.Apoptosis : an international journal on programmed cell death · 2022Pooled it
- Molecular mechanisms of coronary microembolization-induced MINOCA.Basic research in cardiology · 2026Review
- ONC206 demonstrates potent antitumorigenic activity and is a potential novel therapeutic strategy for high-risk medulloblastoma.Neuro-oncology · 2026Article
- Development of a High-Sensitivity Electrochemical Biosensor for Domoic Acid and Its Cellular Impact on Human Stem and Neuron-Like Cells.Food science & nutrition · 2026Article
- Pomiferin protects against sepsis-associated acute liver and kidney injury via inhibition of NF-κB activation, oxidative stress, and cytochrome-c.Scientific reports · 2026Article
- Mitochondria as Inducers of Neutrophil Extracellular Traps.Inflammation · 2026Review
- UBA52 Overexpression Ameliorates Intracerebral Hemorrhage-Associated Neuronal Apoptosis and Mitochondrial Dysfunction: A Protective Role in Neurons.Molecular neurobiology · 2026Article
- Decoding mitochondrial signaling: neutrophil-tumor cell crosstalk in orchestrating cancer progression.Journal of translational medicine · 2026Review
- Pulmonary Exposure to Copper Oxide Nanoparticles Induces Systemic Inflammation, Oxidative Stress, and Prothrombotic Responses in BALB/c Mice.International journal of nanomedicine · 2026Article
- High-Altitude Hypoxia Injury: Systemic Mechanisms and Intervention Strategies on Immune and Inflammatory Responses.Antioxidants (Basel, Switzerland) · 2025Review
- Hepatoprotective effect of diosmetin against thioacetamide-induced liver injury via modulating Bax/NF-κB/caspase-3/Nrf-2/PPARNaunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Raman Monitoring ofInternational journal of molecular sciences · 2025Article
- Article
- Mitochondria as a Disease-Relevant Organelle in Rheumatoid Arthritis: A Key Breakout in Fight Against the Disease.Biomedicines · 2025Review
- Transcriptomic Changes in the Frontal Cortex of Juvenile Pigs with Diet-Induced Metabolic Dysfunction-Associated Liver Disease.Biomedicines · 2025Article
- Efficient Direct Cytosolic Protein Delivery via Protein-Linker Co-engineering.ACS applied materials & interfaces · 2025Article
- Complete Immunophenotypic Reversal of Chronic Lymphocytic Leukaemia With High Dose Parenteral Methylcobalamin: A Case Report and Brief Review of Cobalamin in Cancer.Cancer reports (Hoboken, N.J.) · 2025Review
- Intracellular Biomacromolecule Delivery by Stimuli-Responsive Protein Vesicles Loaded by Hydrophobic Ion Pairing.ACS omega · 2025Article
- Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondria: the hidden engines of traumatic brain injury-driven neurodegeneration.Frontiers in cellular neuroscience · 2025Review
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are evolutionary endosymbionts derived from bacteria. Thus, they bear molecules, such as mitochondrial DNA (mtDNA) that contains CpG DNA repeats and N-formyl peptides (FPs), found in bacteria. Upon cell necrosis or apoptosis, these molecules are released into the interstitial space and the circulation and recognized by the immune cells through the same receptors that recognize pathogen-associated molecular patterns, leading to inflammation. Other mitochondrial molecules are not of bacterial origin, but they may serve as danger-associated molecular patterns (DAMPs) when due to cell injury are translocated into inappropriate compartments. There they are recognized by pattern recognition receptors of the immune cells. Cytochrome c is such a molecule. In this review, experimental and clinical data are presented that confirms cytochrome c release into the extracellular space in pathological conditions characterized by cell death. This indicates that serum cytochrome c, which can be easily measured, may be a clinically useful marker for diagnosing and assessing the severity of such pathological entities. Reasonably, detection of high cytochrome c level into the circulation means release of various other molecules that serves as DAMPs when found extracellularly, the mtDNA and FPs included. Finally, because the release of this universally found compound into the extracellular space makes cytochrome c an ideal molecule to play the role of a DAMP per se, the available experimental and clinical data that support such a role are provided.
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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.