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EET enhances renal function in obese mice resulting in restoration of HO-1-Mfn1/2 signaling, and decrease in hypertension through inhibition of sodium chloride co-transporter.
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data posit MFN1-mediated mitochondrial dynamics in POMC neurons as an intrinsic nutrient-sensing mechanism and unveil an unrecognized link between this subset of neurons and insulin release.
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These results highlight the crucial role of MFN1 in maintaining the competency of the STING pathway.
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Despite apparent mitochondrial dysfunction, hearts deficient in both Mfn1 and Mfn2 are protected against acute myocardial infarction due to impaired mitochondria/sarcoplasmic reticulum tethering.
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We found that mouse embryonic fibroblasts lacking Mfn2 have altered lipid droplet morphology. However, triacylglycerol biosynthesis was not dependent on ER-mitochondrial tethering mediated by mitofusins. Lastly, Mfn2 does not have a role in adipocyte differentiation.
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MFN1 deficiency leads to defects in mitochondrial activity and male infertility.
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Report exposes a novel role for Shh in regulating mitochondrial dynamics and rescue the metabolic profile of tumor cells through regulation of mitofusin 1 and 2.
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Ablating Mfn1 eliminates the cardiac-related lethality of Mff knockout mice.
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Data suggest that mitochondrial fusion and fission events are regulated by four GTPases: Mfn1, Mfn2, OPA1 (optic atrophy 1 protein), and Drp1 (dynamin 1-like protein). [REVIEW]
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Authors present evidence that metabolically challenged mitochondria undergo active fusion to suppress oxidative stress. In response to glucose starvation, mitofusin 1 (MFN1) becomes associated with the protein deacetylase HDAC6.
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These findings suggest that mitochondrial impairment is a very early event in Alzheimer disease pathogenesis and abnormal expression of Mfn1 and Mfn2 caused by excessive intracellular Abeta is the possible molecular mechanism.
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Data identify MFN1 as an ERK target to modulate mitochondrial shape and apoptosis.
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A fine balance of Mfn1 levels is maintained by MARCH5-mediated quality control on acetylated Mfn1.
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Mitochondrial shape governs BAX-induced membrane permeabilization and apoptosis via Mfn1.
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Data unmask an important role for mitochondrial dynamics governed by Mfn1 and Mfn2 in Agrp neurons in central regulation of whole-body energy metabolism.
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Our findings establish that Mfn-1 and Mfn-2 are essential in mediating mitochondrial remodeling during postnatal cardiac development, a time of dramatic transitions in the bioenergetics and growth of the heart.
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Data suggest that Mfn-1 deletion in cardiomyocytes confers protection against reactive oxygen species-induced mitochondrial dysfunction.
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Patterned Purkinje cell degeneration is dependent on caspase activation, leading to the marked decrease of mitofusion 1 in the Harlequin cerebellum.
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Double Mfn-null cells show neither outer nor inner membrane fusion, while mitochondria in OPA1-null cells contain multiple matrix compartments bounded together by a single outer membrane, consistent with uncoupling of outer versus inner membrane fusion.
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results suggest that the heptad repeat region (HR2) of mfn1 functions as a mitochondrial tether before fusion
