ArticleScience advances2022
CLIC4 localizes to mitochondrial-associated membranes and mediates cardioprotection.
Article in Science advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- A cryptic-site ligand stabilizes a non-canonical interface and blocks membrane insertion of the chloride intracellular channel CLIC1.The Journal of biological chemistry · 2026Article
- Transplantation of active mitochondria condensed in liquid-liquid phase-separated hydrogels ameliorates myocardial ischemia-reperfusion injury.Nature communications · 2026Article
- The spatiotemporal dynamics of MAMs: mechanisms, pathologies, and therapeutic rewiring.Cellular & molecular biology letters · 2026Review
- Chloride Intracellular Channel 4 (CLIC4) controls volume regulation in sperm development via Protein Kinase C (PKC).BMC biology · 2026Article
- Dynamic imbalance of mitochondria-associated ER membranes in cardiovascular disease: mechanisms, context dependence and therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- An In Vitro Study of Protein S-Glutathionylation by Members of the CLIC Protein Family.Biomolecules · 2025Article
- Review
- Current research on mitochondria‑associated membranes in cardiovascular diseases (Review).Molecular medicine reports · 2025Review
- Biophysical characterization of anion channels in mitochondrion-endoplasmic-reticulum contact sites.Biophysical journal · 2025Article
- The role of chloride intracellular channel 4 in tumors.Cancer cell international · 2025Review
- Mitochondria-associated endoplasmic reticulum membranes and myocardial ischemia: from molecular mechanisms to therapeutic strategies.Journal of translational medicine · 2025Review
- Chloride intracellular channel CLIC3 mediates fibroblast cellular senescence by interacting with ERK7.Communications biology · 2025Article
- Functional large-conductance calcium and voltage-gated potassium channels in extracellular vesicles act as gatekeepers of structural and functional integrity.Nature communications · 2025Article
- Chloride intracellular channel (CLIC) protein function in S1P-induced Rac1 activation requires membrane localization of the C-terminus, but not thiol-transferase nor ion channel activities.Frontiers in cell and developmental biology · 2025Article
- CLIC1 and CLIC4 demonstrate cell protective antioxidant activity against UV exposure.Frontiers in cell and developmental biology · 2025Article
- Mitochondria-Associated Organelle Crosstalk in Myocardial Ischemia/Reperfusion Injury.Journal of cardiovascular translational research · 2024Review
- ER-mitochondria contact sites regulate hepatic lipogenesis via Ip3r-Grp75-Vdac complex recruiting Seipin.Cell communication and signaling : CCS · 2024Article
- Chloride ions in health and disease.Bioscience reports · 2024Review
- Distinct features of the regenerating heart uncovered through comparative single-cell profiling.Biology open · 2024Article
- Mitochondria-associated endoplasmic reticulum membrane (MAM): a dark horse for diabetic cardiomyopathy treatment.Cell death discovery · 2024Review
Corrections and comments
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Authors and funding
18 authors at 5 institutions in 1 country.
Funding
Abstract
Mitochondrial-associated membranes (MAMs) are known to modulate organellar and cellular functions and can subsequently affect pathophysiology including myocardial ischemia-reperfusion (IR) injury. Thus, identifying molecular targets in MAMs that regulate the outcome of IR injury will hold a key to efficient therapeutics. Here, we found chloride intracellular channel protein (CLIC4) presence in MAMs of cardiomyocytes and demonstrate its role in modulating ER and mitochondrial calcium homeostasis under physiological and pathological conditions. In a murine model, loss of CLIC4 increased myocardial infarction and substantially reduced cardiac function after IR injury. CLIC4 null cardiomyocytes showed increased apoptosis and mitochondrial dysfunction upon hypoxia-reoxygenation injury in comparison to wild-type cardiomyocytes. Overall, our results indicate that MAM-CLIC4 is a key mediator of cellular response to IR injury and therefore may have a potential implication on other pathophysiological processes.
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.