ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
Mechanisms of mitochondrial damage-associated molecular patterns associated with inflammatory response in cardiovascular diseases.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. 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.
- Organelle homeostasis disruption: A driving force in the progression of cardiomyopathy (Review).Experimental and therapeutic medicine · 2026Review
- Cardiovascular Dysfunction in Polycystic Ovary Syndrome: Mitochondrial and Inflammatory Mechanisms.BioMed research international · 2026Review
- Reprogramming the Mitochondrion in Atherosclerosis: Targets for Vascular Protection.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondria as the key to understanding neuroinflammation.Brain : a journal of neurology · 2025Article
- Bioactive Compounds as Modulators of N-Formyl Peptide Signaling in Chronic Diseases.Molecules (Basel, Switzerland) · 2025Review
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.
Funding
Abstract
Cardiovascular diseases (CVDs) continue to be a substantial global healthcare burden despite considerable progress in therapies. The inflammatory response during the progression of CVD has attracted considerable attention. Mitochondria serve as the principal energy source for the heart. In cardiovascular illnesses, mitochondrial homeostasis is disrupted, accompanied by structural and functional impairments. During mitochondrial stress or injury, mitochondrial damage-associated molecular patterns (mtDAMPs), such as mitochondrial DNA, cardiolipin, N-formyl peptide, and adenosine triphosphate, are released to activate pattern recognition receptors and trigger immunological responses. Inflammatory responses mediated by mtDAMPs substantially contribute to the pathophysiology of cardiovascular illnesses. In this review, we discuss the molecular mechanisms by which different mtDAMPs control the inflammatory response, address the pathological consequences of mtDAMPs in inducing or exacerbating the inflammatory response in CVDs, and summarize potential therapeutic targets in relevant experimental studies. Preventing or reducing mtDAMP release may play a role in CVD progression by alleviating the inflammatory response.
Indexed as
Identifiers
39806203What 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.