ReviewJournal of molecular and cellular cardiology2015
Functional implications of mitofusin 2-mediated mitochondrial-SR tethering.
Review in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 81 citations in OpenAlex.
- DNAJB6a deficiency induces tau pathology through IRE1α-Xbp1-induced mitochondria dysfunction.Zoological research · 2026Article
- AMPK-NLRP3 Inflammasome Crosstalk: Structural Insights, Molecular Mechanisms, and Therapeutic Implications for Inflammation and Neuroinflammation.Molecular neurobiology · 2026Review
- Beat-locked ATP microdomains in the sinoatrial node map a Ca2+-timed energetic hierarchy and regional pacemaker roles.The Journal of general physiology · 2026Article
- Demonstration of beat-to-beat, on-demand ATP synthesis in ventricular myocytes reveals sex-specific mitochondrial and cytosolic dynamics.The Journal of physiology · 2026Article
- Disrupted SR-Mitochondria Coupling Drives Ischemia-Reperfusion Vulnerability in the Middle-Aged Rat Heart.Biomedicines · 2026Article
- Energetic microdomains and the vascular control of neuronal and muscle excitability: Toward a unified model.The Journal of physiology · 2026Review
- From homeostasis to pathology, organelle-specific autophagy in skeletal muscle: a PRISMA-ScR scoping review.Frontiers in physiology · 2026Review
- Cardiac SR-Mitochondria Contacts-Impact on Cardiac Physiology and Mitochondrial Fitness.Cells · 2025Review
- Ultrastructure analysis of mitochondria, lipid droplet and sarcoplasmic reticulum apposition in human heart failure.Journal of molecular and cellular cardiology plus · 2025Article
- MAMs and Mitochondrial Quality Control: Overview and Their Role in Alzheimer's Disease.Neurochemical research · 2024Review
- Modifications of Mitochondrial Network Morphology Affect the MAVS-Dependent Immune Response in L929 Murine Fibroblasts during Ectromelia Virus Infection.Pathogens (Basel, Switzerland) · 2024Article
- Mitochondrial network remodeling of the diabetic heart: implications to ischemia related cardiac dysfunction.Cardiovascular diabetology · 2024Review
- Fueling the heartbeat: Dynamic regulation of intracellular ATP during excitation-contraction coupling in ventricular myocytes.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mitochondrial dysfunction is a key link involved in the pathogenesis of sick sinus syndrome: a review.Frontiers in cardiovascular medicine · 2024Review
- Enhanced Mitochondria-SR Tethering Triggers Adaptive Cardiac Muscle Remodeling.Circulation research · 2023Article
- Mitochondrial responses to intracellular CaJournal of neurophysiology · 2023Article
- Premature senescence and cardiovascular disease following cancer treatments: mechanistic insights.Frontiers in cardiovascular medicine · 2023Review
- Mitochondrial dysfunction in heart diseases: Potential therapeutic effects ofFrontiers in pharmacology · 2023Review
- Mitochondria-associated endoplasmic reticulum membranes (MAMs): Possible therapeutic targets in heart failure.Frontiers in cardiovascular medicine · 2023Review
- Disruption of mitochondria-sarcoplasmic reticulum microdomain connectomics contributes to sinus node dysfunction in heart failure.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiomyocyte mitochondria have an intimate physical and functional relationship with sarcoplasmic reticulum (SR). Under normal conditions mitochondrial ATP is essential to power SR calcium cycling that drives phasic contraction/relaxation, and changes in SR calcium release are sensed by mitochondria and used to modulate oxidative phosphorylation according to metabolic need. When perturbed, mitochondrial-SR calcium crosstalk can evoke programmed cell death. Physical proximity and functional interplay between mitochondria and SR are maintained in part through tethering of these two organelles by the membrane protein mitofusin 2 (Mfn2). Here we review and discuss findings from our two laboratories that derive from genetic manipulation of Mfn2 and closely related Mfn1 in mouse hearts and other experimental systems. By comparing the findings of our two independent research efforts we arrive at several conclusions that appear to be strongly supported, and describe a few areas of incomplete understanding that will require further study. In so doing we hope to clarify some misconceptions regarding the many varied roles of Mfn2 as both physical trans-organelle tether and mitochondrial fusion protein. This article is part of a Special Issue entitled "Mitochondria: From Basic Mitochondrial Biology to Cardiovascular Disease."
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.