ReviewCurrent hypertension reports2010
Mitochondrial dysfunction and oxidative damage to sarcomeric proteins.
Review in Current hypertension reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 55 citations in OpenAlex.
- JAK inhibition with tofacitinib rapidly increases contractile force in human skeletal muscle.Life science alliance · 2024Trial
- Exercise based Intervention For Metabolic Inflexibility Linked With Lipid Storage Myopathy Using Innovative CRISPRbioRxiv : the preprint server for biology · 2026Article
- Pimobendan prevents cardiac dysfunction, mitigates cardiac mitochondrial dysfunction, and preserves myocyte ultrastructure in a rat model of mitral regurgitation.BMC veterinary research · 2023Article
- Mitochondrial Integrity Is Critical in Right Heart Failure Development.International journal of molecular sciences · 2023Review
- Article
- Natriuretic Peptide Oligomers Cause Proarrhythmic Metabolic and Electrophysiological Effects in Atrial Myocytes.Circulation. Arrhythmia and electrophysiology · 2022Article
- Involvement of Oxidative Stress in the Development of Subcellular Defects and Heart Disease.Biomedicines · 2022Review
- Metabolic Therapy of Heart Failure: Is There a Future for B Vitamins?International journal of molecular sciences · 2021Review
- Heart Metabolism in Sepsis-Induced Cardiomyopathy-Unusual Metabolic Dysfunction of the Heart.International journal of environmental research and public health · 2021Review
- SERCA2a tyrosine nitration coincides with impairments in maximal SERCA activity in left ventricles from tafazzin-deficient mice.Physiological reports · 2019Article
- Association Between Norepinephrine Levels and Abnormal Iron Status in Patients With Chronic Heart Failure: Is Iron Deficiency More Than a Comorbidity?Journal of the American Heart Association · 2019Observational
- Targeting mitochondrial dysfunction and oxidative stress in heart failure: Challenges and opportunities.Free radical biology & medicine · 2018Review
- Mitochondria and cardiovascular diseases-from pathophysiology to treatment.Annals of translational medicine · 2018Review
- Pyruvate enhancement of cardiac performance: Cellular mechanisms and clinical application.Experimental biology and medicine (Maywood, N.J.) · 2018Review
- Targeting Metabolic Modulation and Mitochondrial Dysfunction in the Treatment of Heart Failure.Diseases (Basel, Switzerland) · 2017Review
- A dose-dependent perturbation in cardiac energy metabolism is linked to radiation-induced ischemic heart disease in Mayak nuclear workers.Oncotarget · 2017Article
- Physiological and pathophysiological reactive oxygen species as probed by EPR spectroscopy: the underutilized research window on muscle ageing.The Journal of physiology · 2016Review
- Article
- Rescue of Heart Failure by Mitochondrial Recovery.International neurourology journal · 2016Review
- Dynamic Myofibrillar Remodeling in Live Cardiomyocytes under Static Stretch.Scientific reports · 2016Article
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
Hypertension is an important risk factor for the development of heart failure. Increased production of reactive oxygen species (ROS) contributes to cardiac dysfunction by activating numerous pro-hypertrophic signaling cascades and damaging the mitochondria, thus setting off a vicious cycle of ROS generation. The way in which oxidative stress leads to exacerbation of systolic and diastolic dysfunction is still unclear, however. In skeletal muscle and ischemic myocardium, increased ROS production causes preferential oxidation of myofibrillar proteins and provides a mechanistic link between oxidative damage and impaired contractility through disruption of actin-myosin interactions, enzymatic functions, calcium sensitivity, and efficiency of cross-bridge cycling. In this review, we summarize recent findings in the fields of heart failure and sarcomere biology and speculate that oxidative damage to myofibrils may contribute to the development of heart failure.
Indexed as
Identifiers
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.