ReviewJournal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi2012
Mitochondrial function in vascular endothelial cell in diabetes.
Review in Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 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
49 citing papers in PubMed, 86 citations in OpenAlex.
- Review
- Insights into the use of oxygen-ozone therapy in ischemic cardiopathy and cardiovascular disease: a role for mitochondria?Medical gas research · 2024Article
- The Role of Endothelial Cell Mitophagy in Age-Related Cardiovascular Diseases.Aging and disease · 2024Review
- Mechanisms involved in the regulation of mitochondrial quality control by PGAM5 in heart failure.Cell stress & chaperones · 2024Review
- Mitochondrial Dysfunction: A Roadmap for Understanding and Tackling Cardiovascular Aging.Aging and disease · 2024Review
- The requirement of the mitochondrial protein NDUFS8 for angiogenesis.Cell death & disease · 2024Article
- Irisin: A Potentially Fresh Insight into the Molecular Mechanisms Underlying Vascular Aging.Aging and disease · 2023Review
- Polydatin improves vascular endothelial function by maintaining mitochondrial homeostasis under high glucose conditions.Scientific reports · 2023Article
- Coronary Microvascular Dysfunction in Diabetes Mellitus: Pathogenetic Mechanisms and Potential Therapeutic Options.Biomedicines · 2022Review
- Molecular mechanisms of coronary microvascular endothelial dysfunction in diabetes mellitus: focus on mitochondrial quality surveillance.Angiogenesis · 2022Review
- Salvianolic acid A promotes mitochondrial biogenesis and function via regulating the AMPK/PGC-1α signaling pathway in HUVECs.Experimental and therapeutic medicine · 2022Article
- Aging of Vascular System Is a Complex Process: The Cornerstone Mechanisms.International journal of molecular sciences · 2022Review
- Inflammatory Mechanisms of Diabetes and Its Vascular Complications.Biomedicines · 2022Review
- Extracellular Vesicles as an Index for Endothelial Injury and Cardiac Dysfunction in a Rodent Model of GDM.International journal of molecular sciences · 2022Article
- Beclin-1/LC3-II dependent macroautophagy was uninfluenced in ischemia-challenged vascular endothelial cells.Genes & diseases · 2022Article
- HuR/Cx40 downregulation causes coronary microvascular dysfunction in type 2 diabetes.JCI insight · 2021Article
- ATPIF1 maintains normal mitochondrial structure which is impaired by CCM3 deficiency in endothelial cells.Cell & bioscience · 2021Article
- Potential role of hydrogen sulfide in diabetes-impaired angiogenesis and ischemic tissue repair.Redox biology · 2020Review
- Article
- Exercise hormone irisin mitigates endothelial barrier dysfunction and microvascular leakage-related diseases.JCI insight · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Micro- and macrovascular complications are commonly seen in diabetic patients and endothelial dysfunction contributes to the development and progression of the complications. Abnormal functions in endothelial cells lead to the increase in vascular tension and atherosclerosis, followed by systemic hypertension as well as increased incidence of ischemia and stroke in diabetic patients. Mitochondria are organelles serving as a source of energy production and as regulators of cell survival (e.g., apoptosis and cell development) and ion homeostasis (e.g., H(+), Ca(2+)). Endothelial mitochondria are mainly responsible for generation of reactive oxygen species (ROS) and maintaining the Ca(2+) concentration in the cytosol. There is increasing evidence that mitochondrial morphological and functional changes are implicated in vascular endothelial dysfunction. Enhanced mitochondrial fission and/or attenuated fusion lead to mitochondrial fragmentation and disrupt the endothelial physiological function. Abnormal mitochondrial biogenesis and disturbance of mitochondrial autophagy increase the accumulation of damaged mitochondria, such as irreversibly depolarized or leaky mitochondria, and facilitate cell death. Augmented mitochondrial ROS production and Ca(2+) overload in mitochondria not only cause the maladaptive effect on the endothelial function, but also are potentially detrimental to cell survival. In this article, we review the physiological and pathophysiological role of mitochondria in endothelial function with special focus on diabetes.
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What OpenQuestion 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 OpenQuestion graph.