ArticleAmerican journal of translational research2021
High uric acid promotes mitophagy through the ROS/CaMKIIδ/Parkin pathway in cardiomyocytes
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Relationship between serum uric acid levels and uric acid lowering therapy with the prognosis of patients with heart failure with preserved ejection fraction: a meta-analysis.Frontiers in cardiovascular medicine · 2024Pooled it
- Uric acid, vitamin D, and left ventricular hypertrophy: Unveiling cardiovascular risks - a retrospective cross-sectional study.Medicine · 2026Article
- Multi-Organ Physiologic Deficits During Exercise Identify Clinical and Molecular Predisposition to Heart Failure with Preserved Ejection Fraction.Circulation · 2026Article
- Urolithin Α modulates inter-organellar communication via calcium-dependent mitophagy to promote healthy ageing.Autophagy · 2025Article
- JAK2/STAT3/HMGCS2 signaling aggravates mitochondrial dysfunction and oxidative stress in hyperuricemia-induced cardiac dysfunction.Molecular medicine (Cambridge, Mass.) · 2025Article
- Association between serum uric acid levels and left ventricular hypertrophy based on electrocardiographic findings: a sex-specific analysis across cardiometabolic diseases.Scientific reports · 2025Article
- Uric acid-induced cardiomyocytic polyamines' insufficience: a potential mechanism mediates cardiomyocytic injury.Frontiers in endocrinology · 2025Article
- L-carnitine attenuated hyperuricemia-associated left ventricular remodeling through ameliorating cardiomyocytic lipid deposition.Frontiers in pharmacology · 2023Article
- Serum uric acid: A risk factor for right ventricular dysfunction and prognosis in heart failure with preserved ejection fraction.Frontiers in endocrinology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIncreasing evidence has suggested that high uric acid (HUA) is closely related to cardiovascular disease (CVD). Mitophagy abnormalities have been reported to participate in multiple pathogenic processes of CVD. However, the potential molecular mechanisms remain unclear. Herein, we investigated the effect of HUA-induced mitophagy and its potential molecular mechanism in cardiomyocytes.
methodsWe established a model of cardiomyocytes induced by HUA
resultsIn the HUA stimulation model, ROS production was increased, and mitochondrial injury indexes (MMP and ATP contents) were decreased. Moreover, these indicators were reversed by 3-MA and KN-93. Under HUA stimulation, the expression of LC3B-II, Parkin, CaMKIIδ and P62 increased significantly. Furthermore, these protein levels were reduced by 3-MA and KN-93.
conclusionHUA can promote cardiomyocyte mitophagy activation through the ROS/CaMKIIδ/parkin pathway axis. This study may provide a new target and theoretical basis for the prevention and treatment of HUA-related metabolic heart disease in the future.
Indexed as
Identifiers
34539992PMC8430116W3200334806What 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.