ArticleNature communications2016
The plasma membrane calcium ATPase 4 signalling in cardiac fibroblasts mediates cardiomyocyte hypertrophy.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 71 citations in OpenAlex.
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- Understanding the Role of Adipokines in Cardiometabolic Dysfunction: A Review of Current Knowledge.Biomolecules · 2025Review
- Expression of foetal gene Pontin is essential in protecting heart against pathological remodelling and cardiomyopathy.Nature communications · 2025Article
- Pharmacological or genetic inhibition of LTCC promotes cardiomyocyte proliferation through inhibition of calcineurin activity.NPJ Regenerative medicine · 2025Article
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- Renalase alleviates salt-induced kidney necroptosis and inflammation.Hypertension research : official journal of the Japanese Society of Hypertension · 2024Article
- The local mechanosensitive response of primary cardiac fibroblasts is influenced by the microenvironment mechanics.Scientific reports · 2024Article
- Cardiac cell senescence: molecular mechanisms, key proteins and therapeutic targets.Cell death discovery · 2024Review
- The transplant rejection response involves neutrophil and macrophage adhesion-mediated trogocytosis and is regulated by NFATc3.Cell death & disease · 2024Article
- CaAnimal cells and systems · 2024Review
- Pharmacological or genetic inhibition of LTCC promotes cardiomyocyte proliferation through inhibition of calcineurin activity.Research square · 2023Article
- Genetic variations in human ATP2B4 gene alter Plasmodium falciparum in vitro growth in RBCs from Gambian adults.Malaria journal · 2023Article
- Micro RNA-411 Expression Improves Cardiac Phenotype Following Myocardial Infarction in Mice.JACC. Basic to translational science · 2022Article
- Treatment with specific and pan-plasma membrane calcium ATPase (PMCA) inhibitors reduces malaria parasite growth in vitro and in vivo.Malaria journal · 2022Article
- The Scientific Rationale for the Introduction of Renalase in the Concept of Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2022Review
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- Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 3 countries.
Funding
Abstract
The heart responds to pathological overload through myocyte hypertrophy. Here we show that this response is regulated by cardiac fibroblasts via a paracrine mechanism involving plasma membrane calcium ATPase 4 (PMCA4). Pmca4 deletion in mice, both systemically and specifically in fibroblasts, reduces the hypertrophic response to pressure overload; however, knocking out Pmca4 specifically in cardiomyocytes does not produce this effect. Mechanistically, cardiac fibroblasts lacking PMCA4 produce higher levels of secreted frizzled related protein 2 (sFRP2), which inhibits the hypertrophic response in neighbouring cardiomyocytes. Furthermore, we show that treatment with the PMCA4 inhibitor aurintricarboxylic acid (ATA) inhibits and reverses cardiac hypertrophy induced by pressure overload in mice. Our results reveal that PMCA4 regulates the development of cardiac hypertrophy and provide proof of principle for a therapeutic approach to treat this condition.
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Registered trials
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