ArticleAmerican journal of translational research2022
ER stress induces myocardial dysfunction and cardiac autophagy in Sestrin2 knockout mice.
Article in American journal of translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 12 citations in OpenAlex.
- A Focus on Natural Autophagy Modulators as Potential Host-Directed Weapons Against Emerging and Re-Emerging Viruses.Medicinal research reviews · 2025Review
- Sestrin2 serves as a scaffold protein to maintain cardiac energy and metabolic homeostasis during pathological stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Review
- Sestrin2 as a Protective Shield against Cardiovascular Disease.International journal of molecular sciences · 2023Review
- Proteomics as a Tool for the Study of Mitochondrial Proteome, Its Dysfunctionality and Pathological Consequences in Cardiovascular Diseases.International journal of molecular sciences · 2023Review
- Protein homeostasis in the aged and diseased heart.The journal of cardiovascular aging · 2023Article
- Sestrin2 in diabetes and diabetic complications.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesSestrin2 is an essential regulator of the cellular adaptive response against various stresses. The endoplasmic reticulum (ER) is critical in maintaining normal cardiac function by controlling intracellular Ca
methodsEchocardiography, contractile function analysis, intracellular Ca
resultsThe study revealed that ER stress caused significant heart dysfunction and cardiotoxicity in the mouse heart and cardiomyocytes. Biochemical analysis indicated enhanced cardiac autophagy mediated by ER stress and AMPK/mTOR activation. Sesn2 knockout exacerbated ER stress-related myocardial dysfunction due to the failed response of cardiac autophagy and AMPK/mTOR pathway activation. Further, pharmacological inhibition of AMPK or autophagy worsened TN-induced cardiac dysfunction.
conclusionTaken together, loss of the Sesn2 protein exacerbates ER stress-induced cardiac dysfunction through the AMPK/mTOR signaling cascade and loss of autophagy response.
Indexed as
Identifiers
36105021PMC9452346W4295904471What 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.