ArticleJournal of molecular and cellular cardiology2019
The cardiomyocyte "redox rheostat": Redox signalling via the AMPK-mTOR axis and regulation of gene and protein expression balancing survival and death.
Article in Journal of molecular and cellular cardiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 37 citations in OpenAlex.
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- The 4E-BPs as Translational Regulators in Neurological Disorders: Molecular Mechanisms and Therapeutic Potential.Molecular neurobiology · 2025Review
- Environmentally Relevant Lead Exposure Alters Cell Morphology and Expression of Neural Hallmarks During SH-SY5Y Neuronal Differentiation.bioRxiv : the preprint server for biology · 2025Article
- Mechanistic role for mTORC1 signaling in profibrotic toxicity of low-dose cadmium.Toxicology and applied pharmacology · 2025Article
- Cellular oxidants and the proteostasis network: balance between activation and destruction.Trends in biochemical sciences · 2024Review
- SGLT2 inhibitors: from glucose-lowering to cardiovascular benefits.Cardiovascular research · 2024Review
- Emerging concepts in heart failure management and treatment: focus on SGLT2 inhibitors in heart failure with preserved ejection fraction.Drugs in context · 2023Review
- Review
- Metformin: Expanding the Scope of Application-Starting Earlier than Yesterday, Canceling Later.International journal of molecular sciences · 2022Review
- Redox Signaling and Sarcopenia: Searching for the Primary Suspect.International journal of molecular sciences · 2021Review
- Emergence of SGLT2 Inhibitors as Powerful Antioxidants in Human Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Qindan Capsule Attenuates Myocardial Hypertrophy and Fibrosis in Pressure Overload-Induced Mice Involving mTOR and TGF-Evidence-based complementary and alternative medicine : eCAM · 2021Article
- NSAIDs-dependent adaption of the mitochondria-proteasome system in immortalized human cardiomyocytes.Scientific reports · 2020Article
- Longevity genes, cardiac ageing, and the pathogenesis of cardiomyopathy: implications for understanding the effects of current and future treatments for heart failure.European heart journal · 2020Article
- Redox Regulation of Cardiac ASK1 (Apoptosis Signal-Regulating Kinase 1) Controls p38-MAPK (Mitogen-Activated Protein Kinase) and Orchestrates Cardiac Remodeling to Hypertension.Hypertension (Dallas, Tex. : 1979) · 2020Article
- Dietary AGEs involvement in colonic inflammation and cancer: insights from an in vitro enterocyte model.Scientific reports · 2020Article
- Long-term caloric restriction activates the myocardial SIRT1/AMPK/PGC-1α pathway in C57BL/6J male mice.Food & nutrition research · 2020Article
- Autophagy and Redox Homeostasis in Parkinson's: A Crucial Balancing Act.Oxidative medicine and cellular longevity · 2020Review
- SGLT inhibitors for improving Healthspan and lifespan.Progress in cardiovascular diseasesReview
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
Abstract
Reactive oxygen species (ROS) play a key role in development of heart failure but, at a cellular level, their effects range from cytoprotection to induction of cell death. Understanding how this is regulated is crucial to develop novel strategies to ameliorate only the detrimental effects. Here, we revisited the fundamental hypothesis that the level of ROS per se is a key factor in the cellular response by applying different concentrations of H
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.