ReviewBiology2024
Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells.
Review in Biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- A Systematic Review of Endothelial Dysfunction in Chronic Venous Disease-Inflammation, Oxidative Stress, and Shear Stress.International journal of molecular sciences · 2025Pooled it
- Molecular biology of vascular bioenergetics rewiring: Mitochondrial protective mechanisms of Piper retrofractum in hypertension and oxidative injury.Molecular biology reports · 2026Review
- From Adaptive Resilience to Catastrophic Systems Collapse: Endothelial Entropy, Ferroptotic Propagation, and the Maternal Point of No Return in Emergency Peripartum Hysterectomy.International journal of molecular sciences · 2026Review
- Butyrate and Butyrate-Producing Bacteria in Cardiovascular-Kidney-Metabolic Syndrome.Antioxidants (Basel, Switzerland) · 2026Review
- Caffeine Sodium Benzoate-Induced Macrophage M1 Polarization Promotes Endothelial Progenitor Cell Dysfunction by Inducing Mitochondrial Dysfunction Via Targeting let-7a-5p/OPA1 Axis.Applied biochemistry and biotechnology · 2026Article
- Role of BMP-7 in Cardiovascular Diseases: From Molecular Mechanisms to Therapeutic Horizons.Current drug targets · 2026Review
- The Examination of Arterial Function and Mechanotransduction Through Brachial Arteries via Flow-Mediated Dilation.Advances in experimental medicine and biology · 2026Review
- When Mitochondria Falter, the Barrier Fails: Mechanisms of Inner Blood-Retinal Barrier (iBRB) Injury and Opportunities for Mitochondria-Targeted Repair.International journal of molecular sciences · 2025Review
- Immune-mediated interactions between sarcopenia and atherosclerosis in aging.Immunity & ageing : I & A · 2025Review
- Article
- Molecular Pathways of Endothelial Dysfunction Induced by Chronic Social Stress and Therapeutic Interventions.Journal of cardiovascular translational research · 2025Review
- The Multifaceted Role of Mitochondria in Angiogenesis.International journal of molecular sciences · 2025Review
- Mitochondrial Dysfunction in Endothelial Cells: A Key Driver of Organ Disorders and Aging.Antioxidants (Basel, Switzerland) · 2025Review
- Pathogenesis of cardiovascular diseases: effects of mitochondrial CF6 on endothelial cell function.Molecular and cellular biochemistry · 2025Review
- From Plaques to Pathways in Alzheimer's Disease: The Mitochondrial-Neurovascular-Metabolic Hypothesis.International journal of molecular sciences · 2024Review
- Oxidized Low-Density Lipoprotein and Its Role in Immunometabolism.International journal of molecular sciences · 2024Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Endothelial dysfunction is associated with several lifestyle-related diseases, including cardiovascular and neurodegenerative diseases, and it contributes significantly to the global health burden. Recent research indicates a link between cardiovascular risk factors (CVRFs), excessive production of reactive oxygen species (ROS), mitochondrial impairment, and endothelial dysfunction. Circulating endothelial progenitor cells (EPCs) are recruited into the vessel wall to maintain appropriate endothelial function, repair, and angiogenesis. After attachment, EPCs differentiate into mature endothelial cells (ECs). Like ECs, EPCs are also susceptible to CVRFs, including metabolic dysfunction and chronic inflammation. Therefore, mitochondrial dysfunction of EPCs may have long-term effects on the function of the mature ECs into which EPCs differentiate, particularly in the presence of endothelial damage. However, a link between CVRFs and impaired mitochondrial function in EPCs has hardly been investigated. In this review, we aim to consolidate existing knowledge on the development of mitochondrial and endothelial dysfunction in the vascular endothelium, place it in the context of recent studies investigating the consequences of CVRFs on EPCs, and discuss the role of mitochondrial dysfunction. Thus, we aim to gain a comprehensive understanding of mechanisms involved in EPC deterioration in relation to CVRFs and address potential therapeutic interventions targeting mitochondrial health to promote endothelial function.
Indexed as
Identifiers
What 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.