ArticleBiology open2012
Mammalian formin Fhod3 plays an essential role in cardiogenesis by organizing myofibrillogenesis.
Article in Biology open, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
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
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- Pooled it
- The formin Fhod3 is required for sarcomere reassembly after mitosis in postnatal cardiomyocytes.Cellular and molecular life sciences : CMLS · 2026Article
- Empowering genetic discoveries and cardiovascular risk assessment by predicting electrocardiograms from genotype.NPJ digital medicine · 2026Article
- FHOD3 deficiency disrupts sarcomere organization and activates caMKII signaling in human stem cell-derived cardiomyocytes.Stem cell research & therapy · 2026Article
- Human formin FHOD3-mediated actin elongation is required for sarcomere integrity in cardiomyocytes.eLife · 2025Article
- Whole-genome sequencing reveals genetic structure and adaptive genes in Nepalese buffalo breeds.BMC genomics · 2024Article
- The expression of the formin Fhod3 in mouse tongue striated muscle.Cell structure and function · 2024Article
- FHOD-1 and profilin protect sarcomeres against contraction-induced deformation> inMolecular biology of the cell · 2024Article
- Fine mapping of candidate effector genes for heart rate.Human genetics · 2024Article
- FHOD-1/profilin-mediated actin assembly protects sarcomeres against contraction-induced deformation inbioRxiv : the preprint server for biology · 2024Article
- Altered Fhod3 expression involved in progressive high-frequency hearing loss via dysregulation of actin polymerization stoichiometry in the cuticular plate.PLoS genetics · 2024Article
- FHODs: Nuclear tethered formins for nuclear mechanotransduction.Frontiers in cell and developmental biology · 2023Review
- Actin-Binding Proteins in Cardiac Hypertrophy.Cells · 2022Review
- Minor hypertrophic cardiomyopathy genes, major insights into the genetics of cardiomyopathies.Nature reviews. Cardiology · 2022Review
- Formins in Human Disease.Cells · 2021Review
- Variant Spectrum of Formin Homology 2 Domain-Containing 3 Gene in Chinese Patients With Hypertrophic Cardiomyopathy.Journal of the American Heart Association · 2021Article
- FHOD formin and SRF promote post-embryonic striated muscle growth through separate pathways in C. elegans.Experimental cell research · 2021Article
- The actin polymerization factor Diaphanous and the actin severing protein Flightless I collaborate to regulate sarcomere size.Developmental biology · 2021Article
- FHOD3 promotes carcinogenesis by regulating RhoA/ROCK1/LIMK1 signaling pathway in medulloblastoma.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2020Article
- Under construction: The dynamic assembly, maintenance, and degradation of the cardiac sarcomere.Journal of molecular and cellular cardiology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart development requires organized integration of actin filaments into the sarcomere, the contractile unit of myofibrils, although it remains largely unknown how actin filaments are assembled during myofibrillogenesis. Here we show that Fhod3, a member of the formin family of proteins that play pivotal roles in actin filament assembly, is essential for myofibrillogenesis at an early stage of heart development. Fhod3(-/-) mice appear normal up to embryonic day (E) 8.5, when the developing heart, composed of premyofibrils, initiates spontaneous contraction. However, these premyofibrils fail to mature and myocardial development does not continue, leading to embryonic lethality by E11.5. Transgenic expression of wild-type Fhod3 in the heart restores myofibril maturation and cardiomyogenesis, which allow Fhod3(-/-) embryos to develop further. Moreover, cardiomyopathic changes with immature myofibrils are caused in mice overexpressing a mutant Fhod3, defective in binding to actin. These findings indicate that actin dynamics, regulated by Fhod3, participate in sarcomere organization during myofibrillogenesis and thus play a crucial role in heart development.
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.