Retraction Notice to: The Ubiquitin Ligase Mul1 Induces Mitophagy in Skeletal Muscle in Response to Muscle-Wasting Stimuli

Lokireddy, Sudarsanareddy; Wijesoma, Isuru W.; Teng, Serena; Bonala, Sabeera; Gluckman, Peter D.; McFarlane, Craig; Sharma, Mridula; Kambadur, Ravi

doi:10.1016/j.cmet.2015.11.010

Cited by 1 publication

(1 citation statement)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several other ubiquitin E3 ligases, such as Gp78, SMURF1, SIAH1, MUL1, and ARIH1, also function in mitophagy regulation. 102 , 103 , 104 Once these ubiquitin E3 ligases are activated on the OMM, they can also ubiquitinate Ub and poly‐Ub chains to mark damaged mitochondria, provide recognition sites for autophagosomes, and help recruit autophagy adaptors. The autophagy adaptor directly interacts with autophagosome light chain 3 (LC3) through its LC3 interaction region (LIR) motif, anchoring Ub‐labeled mitochondria into the autophagosomes.…”

Section: Relationships Between Mitochondria and Rosmentioning

confidence: 99%

Mitochondrial Dysfunction in Oxidative Stress‐Mediated Intervertebral Disc Degeneration

Wang

Zheng

Zhou

et al. 2022

Orthopaedic Surgery

View full text Add to dashboard Cite

Intervertebral disc degeneration (IVDD) is the most common contributor to low back pain (LBP). Recent studies have found that oxidative stress and reactive oxygen species (ROS) play an important role in IVDD. As a by‐product of aerobic respiration, ROS is mainly produced in the mitochondria by the electron transport chain and other mitochondrial located proteins. With the excessive accumulation of ROS, mitochondria are also the primary target of ROS attack in disc cells. A disrupted balance between intracellular ROS production and antioxidant capacity will lead to oxidative stress, which is the key contributor to cell apoptosis, cell senescence, excessive autophagy, and mitochondrial dysfunction. As the pivotal ingredient of oxidative stress, mitochondrial dysfunction manifests as imbalanced mitochondrial dynamics and dysregulated mitophagy. Mitochondria can alter their own dynamics through the process of fusion and fission, so that disabled mitochondria can be separated from the mitochondrial pool. Moreover, mitophagy participates by clearing these dysfunctional mitochondria. Abnormality in any of these processes either increases the production or decreases the clearance of ROS, leading to a vicious cycle that results in the death of intervertebral disc cells in large quantities, combined with degradation of the extracellular matrix and overproduction of matrix metalloproteinase. In this review, we explain the changes in mitochondrial morphology and function during oxidative stress‐mediated IVDD and highlight the important role of mitochondria in this process. Eventually, we summarize the IVDD therapeutic strategies targeting mitochondrial dysfunction based on current understanding of the role of oxidative stress in IVDD.

show abstract

Section: Relationships Between Mitochondria and Rosmentioning

confidence: 99%