ReviewFrontiers in cell and developmental biology2021
Mitochondrial Dysfunction: Cause or Consequence of Vascular Calcification?
Review in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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
47 citing papers in PubMed, 83 citations in OpenAlex.
- Histopathological effect of hypervitaminosis DBMC oral health · 2026Article
- Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026Review
- Pancreatic Exocrine Insufficiency Is Surprisingly Common.Integrative medicine (Encinitas, Calif.) · 2026Article
- Causal inference and mediating pathways of metabolic syndrome on calcific aortic valve stenosis: linkage disequilibrium score regression and two-sample, two-step mendelian randomization study.Journal of cardiothoracic surgery · 2026Article
- Next Generation Calcium Nanomaterials: Disrupting Tumor CaInternational journal of nanomedicine · 2026Review
- Comprehensive Review of Mechanisms and Translational Perspectives on Programmed Cell Death in Vascular Calcification.Biomolecules · 2025Review
- Vascular Smooth Muscle Cell Metabolic Reprogramming in Arteriovenous Fistula Failure.Biomedicines · 2025Review
- PMCell biochemistry and biophysics · 2025Article
- Systemic mitochondrial involvement in mitochondrial myopathy with episodic hyper-creatine kinase-emia: insights from an autopsy case.Journal of neurology · 2025Article
- Hypotaurine Reduces Glucose-Mediated Vascular Calcification.Acta physiologica (Oxford, England) · 2025Article
- Effects of Diethylstilbestrol on the Structure and Function of the Spleen in Male Golden Hamsters.Toxics · 2025Article
- Early detection of Parkinson's disease through multiplex blood and urine biomarkers prior to clinical diagnosis.NPJ Parkinson's disease · 2025Article
- The Role of mtDNA Mutations in Atherosclerosis: The Influence of Mitochondrial Dysfunction on Macrophage Polarization.International journal of molecular sciences · 2025Review
- Circulating PGC-1α and MOTS-c Peptide as Potential Mitochondrial Biomarkers in Patients Undergoing Aortic Valve Replacement.Biologics : targets & therapy · 2025Article
- Oxidative stress and its related epigenetic modifications in vascular calcification: mechanisms and advances.Frontiers in cardiovascular medicine · 2025Review
- Article
- Bibliometric analysis of treatment modalities in calcific aortic valve stenosis.Frontiers in pharmacology · 2025Article
- The Physiological Functions and Therapeutic Potential of Hypoxia-Inducible Factor-1α in Vascular Calcification.Biomolecules · 2024Review
- Association of serum HIF-1α levels with coronary artery calcification in patients of non-dialysis chronic kidney disease.Scientific reports · 2024Article
- Axonal Energy Crisis and Calcium Phosphate Dysregulation as Pathogenesis of Optic Disc Drusen.Aging and disease · 2024Review
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Mitochondria are crucial bioenergetics powerhouses and biosynthetic hubs within cells, which can generate and sequester toxic reactive oxygen species (ROS) in response to oxidative stress. Oxidative stress-stimulated ROS production results in ATP depletion and the opening of mitochondrial permeability transition pores, leading to mitochondria dysfunction and cellular apoptosis. Mitochondrial loss of function is also a key driver in the acquisition of a senescence-associated secretory phenotype that drives senescent cells into a pro-inflammatory state. Maintaining mitochondrial homeostasis is crucial for retaining the contractile phenotype of the vascular smooth muscle cells (VSMCs), the most prominent cells of the vasculature. Loss of this contractile phenotype is associated with the loss of mitochondrial function and a metabolic shift to glycolysis. Emerging evidence suggests that mitochondrial dysfunction may play a direct role in vascular calcification and the underlying pathologies including (1) impairment of mitochondrial function by mineral dysregulation i.e., calcium and phosphate overload in patients with end-stage renal disease and (2) presence of increased ROS in patients with calcific aortic valve disease, atherosclerosis, type-II diabetes and chronic kidney disease. In this review, we discuss the cause and consequence of mitochondrial dysfunction in vascular calcification and underlying pathologies; the role of autophagy and mitophagy pathways in preventing mitochondrial dysfunction during vascular calcification and finally we discuss mitochondrial ROS, DRP1, and HIF-1 as potential novel markers and therapeutic targets for maintaining mitochondrial homeostasis in vascular calcification.
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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.