Mitochondrial anomalies driver to age associated degenerative human ailments

10.2741/4420 ◽  
2016 ◽  
Vol 21 (4) ◽  
pp. 769-793 ◽  
Author(s):  
Pradyumna Kumar Mishra
Keyword(s):  
Mitochondrial Anomalies

Mitochondrial Changes in Cholestasis

1972 ◽  
Vol 30 ◽  
pp. 258-259
Author(s):  
F. G. Zaki
Keyword(s):  
Biliary Obstruction ◽  
Alcoholic Cirrhosis ◽  
Ultrastructural Changes ◽  
List Type ◽  
Common Occurrence ◽  
Extrahepatic Cholestasis ◽  
Mitochondrial Alteration ◽  
Extrahepatic Biliary Obstruction ◽  
Liver Biopsies ◽  
Mitochondrial Anomalies

Alterations of liver cell mitochondria represent pathologic phenomenon of a fundamental nature. Mitochondrial anomalies have been often described in association with cholestasis. In attempt to determine whether a given pattern of mitochondrial alteration has any correlation with the cause of cholestasis, liver biopsies were examined from 38 patients showing :a. extrahepatic cholestasis due to complete or partial extrahepatic biliary obstruction (8 cases proven at operation)b. intrahepatic cholestasis due to drugs (9 cases), viral hepatitis (6 cases) and alcoholic cirrhosis (15 cases).Mitochondria exhibiting ultrastructural changes due to aging or to the ‘wear and teart’ processes were not considered. In this study, the only profound and most prominent mitochondrial deformation was reported on basis of their common occurrence in randomly examined sections.

scholarly journals Diminished O-GlcNAcylation in Alzheimer's disease is strongly correlated with mitochondrial anomalies

2019 ◽  
Vol 1865 (8) ◽  
pp. 2048-2059 ◽  
Author(s):  
Tiffany S. Pinho ◽  
Sónia C. Correia ◽  
George Perry ◽  
António Francisco Ambrósio ◽  
Paula I. Moreira
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Strongly Correlated ◽  
Mitochondrial Anomalies

scholarly journals FUNDC1 interacts with FBXL2 to govern mitochondrial integrity and cardiac function through an IP3R3-dependent manner in obesity

2020 ◽  
Vol 6 (38) ◽  
pp. eabc8561 ◽  
Author(s):  
Jun Ren ◽  
Mingming Sun ◽  
Hao Zhou ◽  
Amir Ajoolabady ◽  
Yuan Zhou ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Ubiquitin Ligase ◽  
High Fat Diet ◽  
Dependent Manner ◽  
Cardiac Damage ◽  
Ubiquitin Ligase Complex ◽  
F Box Protein ◽  
Trisphosphate Receptor ◽  
Type 3 ◽  
Mitochondrial Anomalies

Defective mitophagy is causally linked to obesity complications. Here, we identified an interaction between mitophagy protein FUNDC1 (FUN14 domain containing 1) and receptor subunit of human SCF (SKP1/cullin/F-box protein) ubiquitin ligase complex FBXL2 as a gatekeeper for mitochondrial Ca2+ homeostasis through degradation of IP3R3 (inositol 1,4,5-trisphosphate receptor type 3). Loss of FUNDC1 in FUNDC1−/− mice accentuated high-fat diet–induced cardiac remodeling, functional and mitochondrial anomalies, cell death, rise in IP3R3, and Ca2+ overload. Mass spectrometry and co-immunoprecipitation analyses revealed an interaction between FUNDC1 and FBXL2. Truncated mutants of Fbox (Delta-F-box) disengaged FBXL2 interaction with FUNDC1. Activation or transfection of FBXL2, inhibition of IP3R3 alleviated, whereas disruption of FBXL2 localization sensitized lipotoxicity-induced cardiac damage. FUNDC1 deficiency accelerated and decelerated palmitic acid–induced degradation of FBXL2 and IP3R3, respectively. Our data suggest an essential role for interaction between FUNDC1 and FBXL2 in preserving mitochondrial Ca2+ homeostasis and cardiac function in obese hearts.

Mitochondrial anomalies in a Swiss family with autosomal dominant myoglobinuria

1997 ◽  
Vol 69 (4) ◽  
pp. 365-369 ◽  
Author(s):  
Rémy C. Martin-Du Pan ◽  
Michael A. Morris ◽  
Hervé Favre ◽  
Alain Junod ◽  
Gian-Paolo Pizzolato ◽  
...  
Keyword(s):  
Autosomal Dominant ◽  
Mitochondrial Anomalies

scholarly journals Mitophagy, Mitochondrial Dynamics, and Homeostasis in Cardiovascular Aging

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Ne N. Wu ◽  
Yingmei Zhang ◽  
Jun Ren
Keyword(s):  
Metabolic Diseases ◽  
Mitochondrial Dynamics ◽  
Human Longevity ◽  
Biological Aging ◽  
Telomere Shortening ◽  
Ample Evidence ◽  
Mitochondrial Homeostasis ◽  
Novel Therapeutic Strategies ◽  
Mitochondrial Anomalies

Biological aging is an inevitable and independent risk factor for a wide array of chronic diseases including cardiovascular and metabolic diseases. Ample evidence has established a pivotal role for interrupted mitochondrial homeostasis in the onset and development of aging-related cardiovascular anomalies. A number of culprit factors have been suggested in aging-associated mitochondrial anomalies including oxidative stress, lipid toxicity, telomere shortening, metabolic disturbance, and DNA damage, with recent findings revealing a likely role for compromised mitochondrial dynamics and mitochondrial quality control machinery such as autophagy. Mitochondria undergo consistent fusion and fission, which are crucial for mitochondrial homeostasis and energy adaptation. Autophagy, in particular, mitochondria-selective autophagy, namely, mitophagy, refers to a highly conservative cellular process to degrade and clear long-lived or damaged cellular organelles including mitochondria, the function of which gradually deteriorates with increased age. Mitochondrial homeostasis could be achieved through a cascade of independent but closely related processes including fusion, fission, mitophagy, and mitochondrial biogenesis. With improved health care and increased human longevity, the ever-rising aging society has imposed a high cardiovascular disease prevalence. It is thus imperative to understand the role of mitochondrial homeostasis in the regulation of lifespan and healthspan. Targeting mitochondrial homeostasis should offer promising novel therapeutic strategies against aging-related complications, particularly cardiovascular diseases.

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