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http://dx.doi.org/10.1136/jmg.39.8.e47 | DOI Listing |
To investigate the application of H to alleviate cardiac ischaemia-reperfusion (I/R) injury in a PGC-1α-dependent manner. A rat in vitro myocardial I/R injury model was used, Western blot was used to detect the expression levels of apoptosis markers (Bax, cleaved caspase-3, Bcl), inflammatory factors (IL-1β, TNF-α), mitochondrial fission (DRP1, MFF) and mitochondrial fusion (MFN1, MFN2, OPA1). HE staining was used to observe the effect of H on the myocardial tissue structure injured by I/R.
View Article and Find Full Text PDFPLoS One
November 2024
1st Department of Medicine, University of Pecs Medical School, Pecs, Hungary.
Mitochondria form a dynamic network in cells, regulated by the balance between mitochondrial fusion and fission. The inhibition of mitochondrial fission can have positive effects in acute ischemic/reperfusion injury models by preventing the fall in mitochondrial membrane potential associated with fission processes. However, inhibition of fission in chronic models is disadvantageous because it obstructs the elimination of damaged mitochondrial fragments.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
October 2024
Department of Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States.
Introduction: Reducing Optic Atrophy 1 (OPA1) expression in skeletal muscle in male mice induces Activation Transcription Factor 4 (ATF4) and the integrated stress response (ISR). Additionally, skeletal muscle secretion of Fibroblast Growth Factor 21 (FGF21) is increased, which mediates metabolic adaptations including resistance to diet-induced obesity (DIO) and glucose intolerance in these mice. Although FGF21 induction in this model can be reversed with pharmacological attenuation of ER stress, it remains to be determined if ATF4 is responsible for FGF21 induction and its metabolic benefits in this model.
View Article and Find Full Text PDFInt J Hematol
November 2024
Division of Pediatrics, Faculty of Medicine, University of Miyazaki, 5200, Kihara, Kiyotake, Miyazaki, 889-1692, Japan.
Acute myeloid leukemia (AML) cells are highly dependent on oxidative phosphorylation and the mitochondrial dynamics regulated by fusion-related genes MFN1, MFN2, and OPA1 and fission-related genes DNM1L and MFF. An analysis of previously published gene expression datasets showed that high expression of MFF was significantly associated with poor prognosis in patients with AML. Based on this finding, we investigated the impact of mitochondrial dynamics in AML.
View Article and Find Full Text PDFbioRxiv
August 2024
Department of Biological Chemistry, David Geffen School of Medicine at UCLA.
Mfn2 is a mitochondrial outer membrane fusion protein with the additional role of tethering mitochondria to the ER. Here, we describe a novel connection between Mfn2 and calcium release from mitochondria. We show that Mfn2 controls the mitochondrial inner membrane sodium-calcium exchange protein NCLX, which is a major source for calcium release from mitochondria.
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