Results 51 to 60 of about 63,946 (250)

Insulin-Like Growth Factor I Prevents Cellular Aging via Activation of Mitophagy

open access: yesJournal of Aging Research, 2020
Mitochondrial dysfunction is a hallmark of cellular aging. Mitophagy is a critical mitochondrial quality control mechanism that removes dysfunctional mitochondria and contributes to cell survival. Insulin-like growth factor 1 (IGF-1) promotes survival of
Xuwei Hou   +4 more
doaj   +1 more source

Evaluating mitophagy in embryonic stem cells by using fluorescence-based imaging

open access: yesFrontiers in Cell and Developmental Biology, 2022
Embryonic stem cells (ESCs), which are characterized by the capacity for self-renewal and pluripotency, hold great promise for regenerative medicine. Increasing evidence points to the essential role of mitophagy in pluripotency regulation.
Kun Liu   +15 more
doaj   +1 more source

Copper‐Driven Epithelial Barrier Disruption: A Novel Mechanism of COPD Acute Exacerbations Mediated by the TNF‐α/ATP7A Axis

open access: yesAdvanced Science, EarlyView.
This study reveals a copper‐driven mechanism of COPD acute exacerbations mediated by the TNF‐α/ATP7A axis. TNF‐α suppresses the copper transporter ATP7A via competitive NF‐κB/CREB1/CBP signaling, resulting in intracellular copper accumulation, mitochondrial oxidative stress, and epithelial barrier disruption.
Xinru Xiao   +7 more
wiley   +1 more source

The role of cardiolipin in mitophagy [PDF]

open access: yes, 2014
Mitophagy allows for the removal of damaged and dysfunctional mitochondria from the cell thereby attenuating any deleterious, potentially tumorigenic effects malfunctioning mitochondria may cause.
Galbraith, Laura Catherine Avril
core   +5 more sources

Oxidative stress suppresses PHB2‐mediated mitophagy in β‐cells via the Nrf2/PHB2 pathway

open access: yesJournal of Diabetes Investigation
Aims/Introduction Mitochondrial damage caused by oxidative stress is a main driver of pancreatic β‐cell dysfunction in the pathogenesis of type 2 diabetes mellitus.
Shan Liu   +8 more
doaj   +1 more source

Integrative Multi‐Omics Analysis Reveals a Mitochondrial–Immune Axis Associated With Neoadjuvant Chemotherapy Response in High‐Grade Serous Ovarian Cancer

open access: yesAdvanced Science, EarlyView.
Integrative multi‐omics analysis delineates a mitochondrial–immune axis governing neoadjuvant chemotherapy response in high‐grade serous ovarian cancer. Immune‐active tumors exhibit enhanced B‐cell infiltration and favorable sensitivity, whereas metabolically rewired tumors display oxidative phosphorylation dependency and resistance.
Wei Jiang   +11 more
wiley   +1 more source

Ultrasound‐Activatable Piezoelectric Hydrogel Reprograms Mitochondrial Epigenetics for Osteoarthritis Therapy via the mTOR/GATD3A Axis

open access: yesAdvanced Science, EarlyView.
An ultrasound‐activatable piezoelectric hydrogel reprograms chondrocyte mitochondrial epigenetics via the mTOR/GATD3A axis, clearing damaged mitochondria and alleviating osteoarthritis progression in both mouse models and human cartilage explants. ABSTRACT The avascular nature of cartilage hinders drug delivery for osteoarthritis (OA) therapy.
Hui Zheng   +9 more
wiley   +1 more source

Mechanism and role of mitophagy in the development of severe infection

open access: yesCell Death Discovery
Mitochondria produce adenosine triphosphate and potentially contribute to proinflammatory responses and cell death. Mitophagy, as a conservative phenomenon, scavenges waste mitochondria and their components in the cell. Recent studies suggest that severe
Lixiu Ma, Tianyu Han, Yi-an Zhan
doaj   +1 more source

Parkin-Independent Mitophagy Controls Chemotherapeutic Response in Cancer Cells

open access: yesCell Reports, 2017
Mitophagy is an evolutionarily conserved process that selectively targets impaired mitochondria for degradation. Defects in mitophagy are often associated with diverse pathologies, including cancer.
Elodie Villa   +13 more
doaj   +1 more source

Ubiquitination of ACSL4 by Parkin Suppresses Ferroptosis and Rescues Glucocorticoid‐Induced Bone Loss

open access: yesAdvanced Science, EarlyView.
GCs reduce Parkin, leading to ACSL4 accumulation and PUFA‐phospholipid‐driven ferroptosis in BMSCs, which impairs osteogenesis and promotes adipogenesis, causing GIOP. Parkin restoration (via OE‐Parkin or Parkin‐LNP@DSS6) ubiquitinates and degrades ACSL4, inhibiting ferroptosis, rescuing bone formation, and rescues GIOP bone loss.
Li‐jiang Han   +16 more
wiley   +1 more source

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