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Genome-wide copy number variation association study in anorexia nervosa.
Mol Psychiatry
November 2024
Institute for Molecular Bioscience, University of Queensland, Brisbane, QLD, Australia.
Article Synopsis
- - This study is the first large-scale examination of rare copy number variants (CNVs) in anorexia nervosa (AN), involving data from 7,414 AN cases and 5,044 controls to explore their potential genetic links to the disorder.
- - The researchers investigated both well-known syndromic CNVs and those associated with other diseases but found no significant links between these variants and AN; however, they identified 21 potential CNV regions that may play a role in AN risk, particularly in areas related to metabolic and neurodevelopmental factors.
- - Ultimately, the findings suggest that rare CNVs have a limited impact on the development of AN, aligning it with other psychiatric disorders like bipolar disorder, and indicate that
Deficiency Induced Granulosa Cell Senescence Through STAT1/ATF4 Mediated UPR and STAT1/(ATF4)/HIF1α/BNIP3 Mediated Mitophagy: Prevented by Enocyanin.
Int J Mol Sci
October 2024
School of Basic Medical Science, Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Ningxia Medical University, Yinchuan 750004, China.
Dysfunctional mitochondria producing excessive ROS are the main factors that cause ovarian aging. deficiency causes mitochondrial dysfunction and excessive ROS production, leading to ovarian aging, which is attributed to granulosa cell senescence. The pathway controlling mitochondrial proteostasis and mitochondrial homeostasis of the UPR and mitophagy are closely related with the ROS and cell senescence.
View Article and Find Full Text PDFInner Mitochondrial Membrane Peptidase 2-Like Deletion Aggravates Mitochondrial Apoptosis and Inhibits Autophagy After Hyperglycemia Stroke.
Mol Neurobiol
September 2024
Department of Pathology, School of Basic Medicine, Ningxia Medical University, Yinchuan, 750004, China.
This study investigated the effects of inner mitochondrial membrane peptidase 2-like (Immp2l) deletion on mitochondrial apoptosis and mitochondrial autophagy under hyperglycemic conditions. The middle cerebral artery occlusion (MCAO) model was established in wild-type (WT) mice and Immp2l mice; animals were then exposed to hyperglycemic (induced using 1% streptozotocin) and normoglycemic conditions. Tissues were collected at various time points post-reperfusion.
View Article and Find Full Text PDFIdentification of genetic association between mitochondrial dysfunction and knee osteoarthritis through integrating multi-omics: a summary data-based Mendelian randomization study.
Clin Rheumatol
November 2024
Department of Joint Surgery, HongHui Hospital, Xian Jiaotong University, Xian, Shaanxi, China.
Objective: Association between mitochondrial dysfunction and osteoarthritis (OA) has been consistently investigated, yet their genetic association remains obscure. In this study, mitochondrial-related genes were used as instrumental variables to proxy for mitochondrial dysfunction, and summary data of knee OA (KOA) were used as outcome to examine their genetic association.
Methods: We obtained 1136 mitochondrial-related genes from the human MitoCarta3.
Immp2l Enhances the Structure and Function of Mitochondrial Gpd2 Dehydrogenase.
Int J Mol Sci
January 2024
School of Biotechnology and Biomolecular Sciences, University of New South Wales, Sydney, NSW 2052, Australia.
Article Synopsis
- IMMP2L is a mitochondrial peptidase that removes transit peptides from GPD2 and CYC1, but its effect on their functions is unclear.
- Studies on knockout (KO) mice showed significant decreases in organ size, lean mass, and body weight, along with reduced mitochondrial reactive oxygen species (mitoROS) levels, especially in the kidneys.
- Mitochondrial respiration in the KO mice was compromised for GPD2 and CYC1, differing by tissue and gender, and structural analyses suggested altered interactions within mitochondrial complexes.
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