ReviewFrontiers in cardiovascular medicine2022
The role of mitochondria-associated membranes mediated ROS on NLRP3 inflammasome in cardiovascular diseases.
Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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.
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Who cites it
35 citing papers in PubMed, 49 citations in OpenAlex.
- Unravelling the Therapeutic Potential of Cysteine for Cardiovascular Health.International journal of molecular sciences · 2026Review
- Role of voltage-dependent anion channel 1 in neurodegeneration: Mechanisms, implications, and therapeutic potential.Neural regeneration research · 2026Article
- NADPH oxidases in immunometabolism and disease pathology: mechanistic networks, pollutant triggers, and therapeutic frontiers.Cellular & molecular immunology · 2026Review
- IGF2BP1 modulates ZDHHC5-mediated NLRP3 inflammasome activation to promote mitochondrial damage and foam cell formation of vascular smooth muscle cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- MiR-145-5p Attenuates Doxorubicin-Induced Heart Injury Through Targeting Cardiomyocyte Pyroptosis.The Kaohsiung journal of medical sciences · 2026Article
- Plant natural products targeting NLRP3 inflammasome in Parkinson's disease: Molecular activation and regulation to therapeutics.iScience · 2026Review
- Zinc-Containing Bioactive Glass Programs Macrophage Polarization through Extracellular Traps Regulation for Enhanced Diabetic Wound Healing.Advanced healthcare materials · 2026Article
- The PVAT-MAMs Axis in Atherosclerosis: A Hypothesis-Driven Cross-Scale Conceptual Framework.International journal of molecular sciences · 2026Review
- Taurine attenuatesmSystems · 2026Article
- Review
- Cell death forms in myocardial ischemia-reperfusion injury and their potential clinical applications.Molecular and cellular biochemistry · 2026Review
- Pathophysiology of reactive oxygen species (ROS).Archives of toxicology · 2026Review
- Endothelial mitochondrial homeostasis in the development and progression of atherosclerosis.Frontiers in cardiovascular medicine · 2026Review
- Resveratrol and the NLRP3 Inflammasome: Unlocking the Anti-inflammatory Potential of a Natural Compound.Current pharmaceutical design · 2026Review
- Structural and Functional Alterations of MAMs and Their Immunomodulatory Roles in Sepsis-Induced Lung Injury.Journal of immunology research · 2026Review
- Mitochondrial dysfunction in diabetic cardiomyopathy: a review of pathogenic mechanisms and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Mitochondrial Dysfunction and Metabolic Reprogramming in Chronic Inflammatory Diseases: Molecular Insights and Therapeutic Opportunities.Current issues in molecular biology · 2025Review
- Changes in the endoplasmic reticulum‑mitochondria communication in dermal fibroblasts from early‑stage bipolar disorder patients: Skin‑brain axis as a new route to understand the pathophysiology of mental illness?International journal of molecular medicine · 2025Article
- ENO2 regulates CD4mBio · 2025Article
- The Role of Reactive Oxygen Species (ROS) in Periodontitis: A Potential Therapeutic Target.Immunity, inflammation and disease · 2025Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reactive oxygen species (ROS) metabolism is essential for the homeostasis of cells. Appropriate production of ROS is an important signaling molecule, but excessive ROS production can damage cells. ROS and ROS-associated proteins can act as damage associated molecular pattern molecules (DAMPs) to activate the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in cardiovascular diseases. Previous studies have shown that there are connected sites, termed mitochondria-associated membranes (MAMs), between mitochondria and the endoplasmic reticulum. In cardiovascular disease progression, MAMs play multiple roles, the most important of which is the ability to mediate ROS generation, which further activates the NLPR3 inflammasome, exacerbating the progression of disease. In this review, the following topics will be covered: 1. Molecular structures on MAMs that can mediate ROS generation; 2. Specific mechanisms of molecule-mediated ROS generation and the molecules' roles in cardiovascular disease, 3. The effects of MAMs-mediated ROS on the NLRP3 inflammasome in cardiovascular disease. The purpose of this review is to provide a basis for subsequent clinical treatment development.
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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.