ArticleScientific reports2022
Irisin protects cardiomyocytes against hypoxia/reoxygenation injury via attenuating AMPK mediated endoplasmic reticulum stress.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 29 citations in OpenAlex.
- Hypoxia-induced GRP78 activation disrupts the Fndc5/Irisin axis to accelerate skeletal muscle atrophy.Cell stress & chaperones · 2026Article
- Organ-Specific Regulation of Systemic Aging: Focus on the Brain, Skeletal Muscle, and Gut.Cells · 2026Review
- Single-Cell Transcriptomics of Human Acute Myocardial Infarction Reveals Oxidative Stress-Associated Cardiomyocyte Subpopulations and Candidate Predictive Signatures.Antioxidants (Basel, Switzerland) · 2025Article
- Irisin, the Myokine: Guardian and Mediator in Cardiovascular System.Endocrinology, diabetes & metabolism · 2025Review
- The role of irisin in exercise-induced muscle and metabolic health: a narrative review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Irisin: muscle's novel player in endoplasmic reticulum stress and disease.Molecular and cellular biochemistry · 2025Review
- Irisin attenuates cardiac injury and improves prognosis in rats with hemorrhagic shock by maintaining mitochondrial homeostasis via the AMPK/Drp1 pathway.Frontiers in pharmacology · 2025Article
- Huanglian Jiedu Decoction Alleviates Myocardial Ischemia-Reperfusion Injury via AKT-Mediated Regulation of Endoplasmic Reticulum Stress.Journal of inflammation research · 2025Article
- Irisin Ameliorate Acute Pancreatitis and Acinar Cell Viability through Modulation of the Unfolded Protein Response (UPR) and PPARγ-PGC1α-FNDC5 Pathways.Biomolecules · 2024Article
- Irisin attenuates ventilator-induced diaphragmatic dysfunction by inhibiting endoplasmic reticulum stress through activation of AMPK.Journal of cellular and molecular medicine · 2024Article
- FNDC5/irisin ameliorates bone loss of type 1 diabetes by suppressing endoplasmic reticulum stress‑mediated ferroptosis.Journal of orthopaedic surgery and research · 2024Article
- Review
- Irisin ameliorates myocardial ischemia-reperfusion injury by modulating gut microbiota and intestinal permeability in rats.PloS one · 2023Article
- Irisin enhances longevity by boosting SIRT1, AMPK, autophagy and telomerase.Expert reviews in molecular medicine · 2022Review
- Effect of Hypoxia on Irisin Secretion by Human Cardiomyocytes.In vivo (Athens, Greece)Article
- The Effect of Hypoxia on Irisin Expression in HL-1 Cardiomyocytes.In vivo (Athens, Greece)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endoplasmic reticulum (ER) stress plays a central role in myocardial ischemia/reperfusion (I/R) injury. Irisin has been reported to have protective properties in ischemia disease. In this study, we aimed at investigating whether irisin could alleviate myocardial I/R injury by ER stress attenuation. The in vitro model of hypoxia/reoxygenation (H/R) was established, which resembles I/R in vivo. Cell viability and apoptosis were estimated. Expressions of cleaved caspase-3, cytochrome c, GRP78, pAMPK, CHOP, and eIF2α were assessed by western blot. Our results revealed that pre-treatment with irisin significantly decreased cytochrome c release from mitochondria and caspase-3 activation caused by H/R. Irsin also reduced apoptosis and increased cell viability. These effects were abolished by AMPK inhibitor compound C pre-treatment. Also, GRP78 and CHOP expressions were up-regulated in the H/R group compared to the control group; however, irisin attenuated their expression. The pAMPK level was significantly decreased compared to the control, and this effect could be partly reversed by metformin pre-treatment. These results suggest that ER stress is associated with cell viability decreasing and cardiomyocytes apoptosis induced by H/R. Irisin could efficiently protect cardiomyocytes from H/R-injury via attenuating ER stress and ER stress-induced apoptosis.
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.