ArticleAging cell2014
A dual role for integrin-linked kinase and β1-integrin in modulating cardiac aging.
Article in Aging cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 58 citations in OpenAlex.
- How does a fly die? Insights into ageing from the pathophysiology of Drosophila mortality.GeroScience · 2024Review
- β1 integrins regulate cellular behaviour and cardiomyocyte organization during ventricular wall formation.Cardiovascular research · 2024Article
- Roles of Integrin in Cardiovascular Diseases: From Basic Research to Clinical Implications.International journal of molecular sciences · 2024Review
- What do we mean by "aging"? Questions and perspectives revealed by studies in Drosophila.Mechanisms of ageing and development · 2023Article
- Cardiac fibroblasts and mechanosensation in heart development, health and disease.Nature reviews. Cardiology · 2023Review
- Age-dependent Lamin changes induce cardiac dysfunction via dysregulation of cardiac transcriptional programs.Nature aging · 2023Article
- Mending a broken heart:Disease models & mechanisms · 2021Review
- Targeting Epigenetic Mechanisms in Vascular Aging.Frontiers in cardiovascular medicine · 2021Review
- Prolonged Exposure to Microgravity Reduces Cardiac Contractility and Initiates Remodeling in Drosophila.Cell reports · 2020Article
- Mechanosensing dysregulation in the fibroblast: A hallmark of the aging heart.Ageing research reviews · 2020Review
- Interleukin-10 Deficiency Alters Endothelial Progenitor Cell-Derived Exosome Reparative Effect on Myocardial Repair via Integrin-Linked Kinase Enrichment.Circulation research · 2020Article
- Cbl-Associated Protein CAP contributes to correct formation and robust function of the Drosophila heart tube.PloS one · 2020Article
- Integrins in disguise - mechanosensors inMicrobial cell (Graz, Austria) · 2019Review
- As time flies by: Investigating cardiac aging in the short-lived Drosophila model.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Organelle aging: Lessons from model organisms.Journal of genetics and genomics = Yi chuan xue bao · 2019Review
- Hyperphosphatemia Promotes Senescence of Myoblasts by Impairing Autophagy Through Ilk Overexpression, A Possible Mechanism Involved in Sarcopenia.Aging and disease · 2018Article
- Quantitative temporal analysis of protein dynamics in cardiac remodeling.Journal of molecular and cellular cardiology · 2018Article
- The impact of SPARC on age-related cardiac dysfunction and fibrosis in Drosophila.Experimental gerontology · 2018Article
- Distinct domains in the matricellular protein Lonely heart are crucial for cardiac extracellular matrix formation and heart function inThe Journal of biological chemistry · 2018Article
- Influence of hippocampal niche signals on neural stem cell functions during aging.Cell and tissue research · 2018Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
Abstract
Cardiac performance decreases with age, which is a major risk factor for cardiovascular disease and mortality in the aging human population, but the molecular mechanisms underlying cardiac aging are still poorly understood. Investigating the role of integrin-linked kinase (ilk) and β1-integrin (myospheroid, mys) in Drosophila, which colocalize near cardiomyocyte contacts and Z-bands, we find that reduced ilk or mys function prevents the typical changes of cardiac aging seen in wildtype, such as arrhythmias. In particular, the characteristic increase in cardiac arrhythmias with age is prevented in ilk and mys heterozygous flies with nearly identical genetic background, and they live longer, in line with previous findings in Caenorhabditis elegans for ilk and in Drosophila for mys. Consistent with these findings, we observed elevated β1-integrin protein levels in old compared with young wild-type flies, and cardiac-specific overexpression of mys in young flies causes aging-like heart dysfunction. Moreover, moderate cardiac-specific knockdown of integrin-linked kinase (ILK)/integrin pathway-associated genes also prevented the decline in cardiac performance with age. In contrast, strong cardiac knockdown of ilk or ILK-associated genes can severely compromise cardiac integrity, including cardiomyocyte adhesion and overall heart function. These data suggest that ilk/mys function is necessary for establishing and maintaining normal heart structure and function, and appropriate fine-tuning of this pathway can retard the age-dependent decline in cardiac performance and extend lifespan. Thus, ILK/integrin-associated signaling emerges as an important and conserved genetic mechanism in longevity, and as a new means to improve age-dependent cardiac performance, in addition to its vital role in maintaining cardiac integrity.
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Registered trials
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