ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022
ER, Mitochondria, and ISR Regulation by mt-HSP70 and ATF5 upon Procollagen Misfolding in Osteoblasts.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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
28 citing papers in PubMed, 32 citations in OpenAlex.
- Inhibition of EED enhances osteogenic differentiation and bone formation: a potential therapeutic strategy for osteogenesis imperfecta.JBMR plus · 2026Article
- Heat shock protein-mediated remodeling of the bone immune microenvironment: mechanisms and precision therapeutic strategies for osteoporosis.Journal of translational medicine · 2026Review
- Vitamin B3 suppressesTranslational cancer research · 2026Article
- Current advances of bone homeostasis imbalance in the cause of hereditary metabolic bone diseases.EFORT open reviews · 2026Review
- Single-cell transcriptomics showed that maternal polychlorinated biphenyl exposure dysregulated cell type-specific metabolic responses in the livers of female mouse offsprings.Drug metabolism and disposition: the biological fate of chemicals · 2026Article
- A New Perspective on Osteogenesis Imperfecta: From Cellular Mechanisms to the Systemic Impact of Collagen Dysfunction.International journal of molecular sciences · 2026Review
- Molecular drivers of osteogenesis imperfecta: a cellular and extracellular collagen disease.Clinical science (London, England : 1979) · 2025Review
- The Role of Osteoblasts in Phenotypic Variability of Dominant Osteogenesis Imperfecta: Evidence from Patients and Murine Models.International journal of molecular sciences · 2025Article
- LC3 and GABARAP independent autophagy of misfolded procollagen in mouse osteoblasts.Autophagy · 2025Article
- Osteogenesis Imperfecta: A Look into the Cerebellum of the Brtl Murine Model.Molecular neurobiology · 2025Article
- Failed Cellular Surveillance Enables Pathogenic Matrix Deposition in abioRxiv : the preprint server for biology · 2025Article
- Apolipoprotein E is a marker of all chondrocytes in the growth plate resting zone.Bone research · 2025Article
- Comprehensive Review of Osteogenesis Imperfecta: Current Treatments and Future Innovations.Human gene therapy · 2025Review
- Effects of stress on bone health in children.Frontiers in endocrinology · 2025Review
- Cellular and Molecular Effects of the Bruck Syndrome-Associated Mutation in theInternational journal of molecular sciences · 2024Article
- Extra-Skeletal Manifestations in Osteogenesis Imperfecta Mouse Models.Calcified tissue international · 2024Review
- Update on the Genetics of Osteogenesis Imperfecta.Calcified tissue international · 2024Review
- The Role of Mitochondrial Homeostasis in Mesenchymal Stem Cell Therapy-Potential Implications in the Treatment of Osteogenesis Imperfecta.Pharmaceuticals (Basel, Switzerland) · 2024Review
- ER procollagen storage defect without coupled unfolded protein response drives precocious arthritis.Life science alliance · 2024Article
- Apolipoprotein E is a novel marker for chondrocytes in the growth plate resting zone.Research square · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
Cellular response to protein misfolding underlies multiple diseases. Collagens are the most abundant vertebrate proteins, yet little is known about cellular response to misfolding of their procollagen precursors. Osteoblasts (OBs)-the cells that make bone-produce so much procollagen that it accounts for up to 40% of mRNAs in the cell, which is why bone bears the brunt of mutations causing procollagen misfolding in osteogenesis imperfecta (OI). The present study of a G610C mouse model of OI by multiple transcriptomic techniques provides first solid clues to how OBs respond to misfolded procollagen accumulation in the endoplasmic reticulum (ER) and how this response affects OB function. Surprisingly, misfolded procollagen escapes the quality control in the ER lumen and indirectly triggers the integrated stress response (ISR) through other cell compartments. In G610C OBs, the ISR is regulated by mitochondrial HSP70 (mt-HSP70) and ATF5 instead of their BIP and ATF4 paralogues, which normally activate and regulate ISR to secretory protein misfolding in the ER. The involvement of mt-HSP70 and ATF5 together with other transcriptomic findings suggest that mitochondria might initiate the ISR upon disruption of ER-mitochondria connections or might respond to the ISR activated by a yet unknown sensor.
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.