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Cited by 189

The DOI matches its Crossref record; 8 of the 8 references it cites were found in a registry or an index.

Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction

Open access
Hall, A R, Burke, N, Dongworth, R K, Kalkhoran, S B, Dyson, A, Vicencio, J M, Dorn, G W, Yellon, D M, Hausenloy, D J·2016·Cell Death & Disease
DOI 10.1038/cddis.2016.139
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Abstract

Mitochondria alter their shape by undergoing cycles of fusion and fission. Changes in mitochondrial morphology impact on the cellular response to stress, and their interactions with other organelles such as the sarcoplasmic reticulum (SR). Inhibiting mitochondrial fission can protect the heart against acute ischemia/reperfusion (I/R) injury. However, the role of the mitochondrial fusion proteins, Mfn1 and Mfn2, in the response of the adult heart to acute I/R injury is not clear, and is investigated in this study. To determine the effect of combined Mfn1/Mfn2 ablation on the susceptibility to acute myocardial I/R injury, cardiac-specific ablation of both Mfn1 and Mfn2 (DKO) was initiated in mice aged 4–6 weeks, leading to knockout of both these proteins in 8–10-week-old animals. This resulted in fragmented mitochondria (electron microscopy), decreased mitochondrial respiratory function (respirometry), and impaired myocardial contractile function (echocardiography). In DKO mice subjected to in vivo regional myocardial ischemia (30 min) followed by 24 h reperfusion, myocardial infarct size (IS, expressed as a % of the area-at-risk) was reduced by 46% compared with wild-type (WT) hearts. In addition, mitochondria from DKO animals had decreased MPTP opening susceptibility (assessed by Ca 2+-induced mitochondrial swelling), compared with WT hearts. Mfn2 is a key mediator of mitochondrial/SR tethering, and accordingly, the loss of Mfn2 in DKO hearts reduced the number of interactions measured between these organelles (quantified by proximal ligation assay), attenuated mitochondrial calcium overload (Rhod2 confocal microscopy), and decreased reactive oxygen species production (DCF confocal microscopy) in response to acute I/R injury. No differences in isolated mitochondrial ROS emissions (Amplex Red) were detected in response to Ca 2+ and Antimycin A, further implicating disruption of mitochondria/SR tethering as the protective mechanism. In summary, despite apparent mitochondrial dysfunction, hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction due to impaired mitochondria/SR tethering.

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Metadata

Authors
Hall, A. R., Burke, N., Dongworth, R. K., Kalkhoran, S. B., Dyson, A., Vicencio, J. M., Dorn, G. W., Yellon, D. M., & Hausenloy, D. J.
Venue
Cell Death & Disease
Publisher
Springer Science and Business Media LLC
Published
2016-05-26
Volume
7
Issue
5
Pages
e2238-e2238
ISSN
2041-4889 (ISSN-L)
DOI
10.1038/cddis.2016.139
OpenAlex
W2400538386
Cited by
189
References
8
FWCI
12.25
Type
journal article
Language
en
Open access
gold

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CoChat. (2026). Citation check: Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction. https://app.cochat.ai/papers/10.1038/cddis.2016.139
The paper
Hall, A. R., Burke, N., Dongworth, R. K., Kalkhoran, S. B., Dyson, A., Vicencio, J. M., Dorn, G. W., Yellon, D. M., & Hausenloy, D. J. (2016). Hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction. Cell Death & Disease. https://doi.org/10.1038/cddis.2016.139

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.