ArticleResearch (Washington, D.C.)2023
LonP1 Links Mitochondria-ER Interaction to Regulate Heart Function.
Article in Research (Washington, D.C.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 33 citations in OpenAlex.
- Mitochondrial quality control in health and disease: Updates 2026.Chinese medical journal · 2026Review
- A multilayered stress-response circuit: The mammalian mitochondrial UPR.The FEBS journal · 2026Review
- Mitochondria‑endoplasmic reticulum contact site nexus: Molecular integration, disease pathogenesis and therapeutic opportunities (Review).International journal of molecular medicine · 2026Review
- Reprogramming Mitochondrial Adaptation: LONP1 at the Crossroads of Proteostasis, Metabolism, and Disease.Antioxidants (Basel, Switzerland) · 2026Review
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- Mitochondria-associated endoplasmic reticulum membranes: Emerging regulators of cardiac microvascular ischemia/reperfusion injury (Review).International journal of molecular medicine · 2026Review
- Role of LONP1 in human diseases: molecular mechanisms and therapeutic potential.Cellular & molecular biology letters · 2026Review
- Review
- LXRα/SCD1-Mediated Endoplasmic Reticulum-Mitochondria Crosstalk in Inhibiting Neuronal Ferroptosis after Spinal Cord Injury.Research (Washington, D.C.) · 2026Article
- The core mechanism of traditional Chinese medicine in improving myocardial fibrosis: restoring the dynamic balance of mitochondrial quality control.Frontiers in cardiovascular medicine · 2026Review
- Beyond the genome: clinical challenges in diagnosingFrontiers in cell and developmental biology · 2026Article
- Proteasomal inhibition compromises microvascular integrity via distinct effects on non-immune endothelial cells and immune cells.Frontiers in immunology · 2026Article
- Dysregulation of placental mitochondrial structure dynamics and clearance in maternal obesity and gestational diabetes.Placenta · 2025Article
- Genetic and Multi-Omics Insights Into Monocyte Pantothenate-Mediated Protection in Acute Respiratory Distress Syndrome.Journal of cellular and molecular medicine · 2025Article
- Mitochondrial quality control in cardiomyocytes: safeguarding the heart against disease and ageing.Nature reviews. Cardiology · 2025Review
- Mitochondrial ultrastructural pathology in diabetic cardiomyopathy: integrated analysis via scanning electron microscopy and 3D visualization imaging.Cardiovascular diabetology · 2025Article
- Current research on mitochondria‑associated membranes in cardiovascular diseases (Review).Molecular medicine reports · 2025Review
- Peste des petits ruminants virus (PPRV) induces ferroptosis via LONP1-mediated mitochondrial GPX4 degradation in cell culture.Journal of virology · 2025Article
- Modulation of Lonp1 Activity by Small Compounds.Biomolecules · 2025Review
- Palladium Nanoparticles Degrade Advanced Glycation End Products via Valosin-Containing Protein Mediated Autophagy to Attenuate High-Glucose/High-Fat-Induced Intervertebral Disc Degeneration.Exploration (Beijing, China) · 2025Article
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interorganelle contacts and communications are increasingly recognized to play a vital role in cellular function and homeostasis. In particular, the mitochondria-endoplasmic reticulum (ER) membrane contact site (MAM) is known to regulate ion and lipid transfer, as well as signaling and organelle dynamics. However, the regulatory mechanisms of MAM formation and their function are still elusive. Here, we identify mitochondrial Lon protease (LonP1), a highly conserved mitochondrial matrix protease, as a new MAM tethering protein. The removal of LonP1 substantially reduces MAM formation and causes mitochondrial fragmentation. Furthermore, deletion of LonP1 in the cardiomyocytes of mouse heart impairs MAM integrity and mitochondrial fusion and activates the unfolded protein response within the ER (UPR
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.