ArticleJCSM rapid communications
Cancer-induced Cardiac Atrophy Adversely Affects Myocardial Redox State and Mitochondrial Oxidative Characteristics.
Article in JCSM rapid communications. 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, 22 citations in OpenAlex.
- Myocardial fibrosis and strain impairment in treatment-naïve cancer patients: insights into cancer-related myocardial remodeling from a prospective case-control CMR study.La Radiologia medica · 2026Article
- Intracerebral Administration of Hydrogen Sulfide Impairs Bioenergetics, Redox Status and Mitochondrial Quality Control in Rat Striatum.Neurotoxicity research · 2025Article
- Disturbances in mitochondrial quality control and mitochondria-lysosome contact underlie the cerebral cortex and heart damage of mucopolysaccharidosis type II mice.Metabolic brain disease · 2025Article
- Disturbances in mitochondrial bioenergetics and control quality and unbalanced redox homeostasis in the liver of a mouse model of mucopolysaccharidosis type II.Molecular and cellular biochemistry · 2025Article
- Esculetin inhibits the PI3K/Akt/mTOR pathway and enhances anti-colorectal cancer activity via binding to ENO1.Frontiers in pharmacology · 2025Article
- Does Myocardial Atrophy Represent Anti-Arrhythmic Phenotype?Biomedicines · 2022Review
- PGC-1α overexpression is not sufficient to mitigate cancer cachexia in either male or female mice.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2022Article
- Cardiac Remodeling in Cancer-Induced Cachexia: Functional, Structural, and Metabolic Contributors.Cells · 2022Review
- Review
- Review
- Review
- Sex Differences in Cardiac Pathology of SARS-CoV2 Infected andFrontiers in cardiovascular medicine · 2022Article
- Integrative analysis identifies potential ferroptosis-related genes of hypoxia adaptation in yak.Frontiers in veterinary science · 2022Article
- Cardiac myocyte intrinsic contractility and calcium handling deficits underlie heart organ dysfunction in murine cancer cachexia.Scientific reports · 2021Article
- Nutrition challenges of cancer cachexia.JPEN. Journal of parenteral and enteral nutrition · 2021Review
- Cardiac dysfunction from cancer and cancer therapy: new pathways for the prevention of late cardiotoxicity.Basic research in cardiology · 2021Article
- Tumor burden negatively impacts protein turnover as a proteostatic process in noncancerous liver, heart, and muscle, but not brain.Journal of applied physiology (Bethesda, Md. : 1985) · 2021Article
- Development and progression of cancer cachexia: Perspectives from bench to bedside.Sports medicine and health science · 2020Article
- Mitochondrial Function and Protein Turnover in the Diaphragm are Altered in LLC Tumor Model of Cancer Cachexia.International journal of molecular sciences · 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
10 authors at 1 institution in 1 country.
Funding
Abstract
Cachexia presents in 80% of advanced cancer patients; however, cardiac atrophy in cachectic patients receives little attention. This cardiomyopathy contributes to increased occurrence of adverse cardiac events compared to age-matched population norms. Research on cardiac atrophy has focused on remodeling; however, alterations in metabolic properties may be a primary contributor. PURPOSE: Determine how cancer-induced cardiac atrophy alters mitochondrial turnover, mitochondrial mRNA translation machinery and
methodsLewis lung carcinoma (LLC) tumors were implanted in C57BL6/J mice and grown for 28days to induce cardiac atrophy. Endogenous metabolic species, and markers of mitochondrial function were assessed. H9c2 cardiomyocytes were cultured in LLC-conditioned media with(out) the antioxidant MitoTempo. Cells were analyzed for ROS, oxidative capacity, and hypoxic resistance.
resultsLLC heart weights were ~10% lower than controls. LLC hearts demonstrated ~15% lower optical redox ratio (FAD/FAD+NADH) compared to PBS controls. When compared to PBS, LLC hearts showed ~50% greater COX-IV and VDAC, attributed to ~50% lower mitophagy markers. mt-mRNA translation machinery was elevated similarly to markers of mitochondrial content. mitochondrial DNA-encoded Cytb was ~30% lower in LLC hearts. ROS scavengers GPx-3 and GPx-7 were ~50% lower in LLC hearts. Treatment of cardiomyocytes with LLC-conditioned media resulted in higher ROS (25%), lower oxygen consumption rates (10% at basal, 75% at maximal), and greater susceptibility to hypoxia (~25%) -- which was reversed by MitoTempo.
conclusionThese results substantiate metabolic cardiotoxic effects attributable to tumor-associated factors and provide insight into interactions between mitochondrial mRNA translation, ROS mitigation, oxidative capacity and hypoxia resistance.
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.