ReviewJournal of cellular and molecular medicine2012
Measuring passive myocardial stiffness in Drosophila melanogaster to investigate diastolic dysfunction.
Review in Journal of cellular and molecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 30 citations in OpenAlex.
- The mTOR signaling pathway in cardiac aging.The journal of cardiovascular aging · 2023Article
- Regular Exercise Rescues Heart Function Defects and Shortens the Lifespan ofInternational journal of environmental research and public health · 2022Article
- As time flies by: Investigating cardiac aging in the short-lived Drosophila model.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Preserved cardiac function by vinculin enhances glucose oxidation and extends health- and life-span.APL bioengineering · 2018Article
- Extracellular matrix downregulation in the Drosophila heart preserves contractile function and improves lifespan.Matrix biology : journal of the International Society for Matrix Biology · 2017Article
- Dissecting the Role of the Extracellular Matrix in Heart Disease: Lessons from the Drosophila Genetic Model.Veterinary sciences · 2017Review
- Expression patterns of cardiac aging in Drosophila.Aging cell · 2017Article
- Modest overexpression of FOXO maintains cardiac proteostasis and ameliorates age-associated functional decline.Aging cell · 2017Article
- Concise Review: Organ Engineering: Design, Technology, and Integration.Stem cells (Dayton, Ohio) · 2017Review
- Molecular mechanisms of heart failure: insights from Drosophila.Heart failure reviews · 2017Review
- Mechanical Regulation of Cardiac Aging in Model Systems.Circulation research · 2016Review
- Genetic manipulation of cardiac ageing.The Journal of physiology · 2016Review
- On the Morphology of the Drosophila Heart.Journal of cardiovascular development and disease · 2016Review
- Review
- The (dys)functional extracellular matrix.Biochimica et biophysica acta · 2015Review
- Vinculin network-mediated cytoskeletal remodeling regulates contractile function in the aging heart.Science translational medicine · 2015Article
- Colored polydimethylsiloxane micropillar arrays for high throughput measurements of forces applied by genetic model organisms.Biomicrofluidics · 2015Article
- Interplay of matrix stiffness and protein tethering in stem cell differentiation.Nature materials · 2014Article
- Methods to assess Drosophila heart development, function and aging.Methods (San Diego, Calif.) · 2014Review
- A dual role for integrin-linked kinase and β1-integrin in modulating cardiac aging.Aging cell · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Aging is marked by a decline in LV diastolic function, which encompasses abnormalities in diastolic relaxation, chamber filling and/or passive myocardial stiffness. Genetic tractability and short life span make Drosophila melanogaster an ideal organism to study the effects of aging on heart function, including senescent-associated changes in gene expression and in passive myocardial stiffness. However, use of the Drosophila heart tube to probe deterioration of diastolic performance is subject to at least two challenges: the extent of genetic homology to mammals and the ability to resolve mechanical properties of the bilayered fly heart, which consists of a ventral muscle layer that covers the contractile cardiomyocytes. Here, we argue for widespread use of Drosophila as a novel myocardial aging model by (1) describing diastolic dysfunction in flies, (2) discussing how critical pathways involved in dysfunction are conserved across species and (3) demonstrating the advantage of an atomic force microscopy-based analysis method to measure stiffness of the multilayered Drosophila heart tube versus isolated myocytes from other model systems. By using powerful Drosophila genetic tools, we aim to efficiently alter changes observed in factors that contribute to diastolic dysfunction to understand how one might improve diastolic performance at advanced ages in humans.
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.