ArticleOpen biology2016
Autophagy protects cardiomyocytes from the myocardial ischaemia-reperfusion injury through the clearance of CLP36.
Article in Open biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 36 citations in OpenAlex.
- Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.ESC heart failure · 2025Review
- The multifaceted role of autophagy and mitophagy in cardiovascular health and disease.Autophagy reports · 2025Review
- β-hydroxybutyrate administered at reperfusion reduces infarct size and preserves cardiac function by improving mitochondrial function through autophagy in male mice.Journal of molecular and cellular cardiology · 2024Article
- Crosstalk between myocardial autophagy and sterile inflammation in the development of heart failure.Autophagy reports · 2024Review
- Autophagy in Heart Failure: Insights into Mechanisms and Therapeutic Implications.Journal of cardiovascular development and disease · 2023Review
- Chaperone-mediated autophagy protects cardiomyocytes against hypoxic-cell death.American journal of physiology. Cell physiology · 2022Article
- The role of autophagy in cardiovascular pathology.Cardiovascular research · 2022Review
- Recent Advances on Drug Development and Emerging Therapeutic Agents Through Targeting Cellular Homeostasis for Ageing and Cardiovascular Disease.Frontiers in aging · 2022Review
- Association of miR-192-5p with Atherosclerosis and its Effect on Proliferation and Migration of Vascular Smooth Muscle Cells.Molecular biotechnology · 2021Article
- Mitochondrial Quality Control in Cardiac-Conditioning Strategies against Ischemia-Reperfusion Injury.Life (Basel, Switzerland) · 2021Review
- Review
- Activation of Autophagic Flux Blunts Cardiac Ischemia/Reperfusion Injury.Circulation research · 2021Article
- Review
- The Role of Sinusoidal Endothelial Cells in the Axis of Inflammation and Cancer Within the Liver.Frontiers in physiology · 2020Review
- HDAC inhibition induces autophagy and mitochondrial biogenesis to maintain mitochondrial homeostasis during cardiac ischemia/reperfusion injury.Journal of molecular and cellular cardiology · 2019Article
- Functional variants of the ATG7 gene promoter in acute myocardial infarction.Molecular genetics & genomic medicine · 2018Article
- PARP1 promote autophagy in cardiomyocytes via modulating FoxO3a transcription.Cell death & disease · 2018Article
- Macroautophagy and Chaperone-Mediated Autophagy in Heart Failure: The Known and the Unknown.Oxidative medicine and cellular longevity · 2018Review
- An Intervention Target for Myocardial Fibrosis: Autophagy.BioMed research international · 2018Review
- Autophagy attenuates endothelial-to-mesenchymal transition by promoting Snail degradation in human cardiac microvascular endothelial cells.Bioscience reports · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular disease (CVD) is the leading cause of the death worldwide. An increasing number of studies have found that autophagy is involved in the progression or prevention of CVD. However, the precise mechanism of autophagy in CVD, especially the myocardial ischaemia-reperfusion injury (MI/R injury), is unclear and controversial. Here, we show that the cardiomyocyte-specific disruption of autophagy by conditional knockout of Atg7 leads to severe contractile dysfunction, myofibrillar disarray and vacuolar cardiomyocytes. A negative cytoskeleton organization regulator, CLP36, was found to be accumulated in Atg7-deficient cardiomyocytes. The cardiomyocyte-specific knockout of Atg7 aggravates the MI/R injury with cardiac hypertrophy, contractile dysfunction, myofibrillar disarray and severe cardiac fibrosis, most probably due to CLP36 accumulation in cardiomyocytes. Altogether, this work reveals autophagy may protect cardiomyocytes from the MI/R injury through the clearance of CLP36, and these findings define a novel relationship between autophagy and the regulation of stress fibre in heart.
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.