Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 18, 2025
Language: Английский
Molecular Neurodegeneration, Journal Year: 2023, Volume and Issue: 18(1)
Published: Nov. 11, 2023
Abstract Mitochondrial dysfunction is strongly implicated in the etiology of idiopathic and genetic Parkinson’s disease (PD). However, strategies aimed at ameliorating mitochondrial dysfunction, including antioxidants, antidiabetic drugs, iron chelators, have failed disease-modification clinical trials. In this review, we summarize cellular determinants impairment electron transport chain complex 1, increased oxidative stress, disturbed quality control mechanisms, bioenergetic deficiency. addition, outline pathways to neurodegeneration current context PD pathogenesis, review past treatment an attempt better understand why translational efforts thus far been unsuccessful.
Language: Английский
Citations
94
Biochemical Pharmacology, Journal Year: 2022, Volume and Issue: 199, P. 115011 - 115011
Published: March 19, 2022
Language: Английский
Citations
77
Frontiers in Aging Neuroscience, Journal Year: 2022, Volume and Issue: 14
Published: June 20, 2022
Parkinson's disease (PD) is one of the most common neurodegenerative movement disorders worldwide. There are currently no cures or preventative treatments for PD. Emerging evidence indicates that mitochondrial dysfunction closely associated with pathogenesis sporadic and familial Because dopaminergic neurons have high energy demand, cells affected by PD exhibit promotes disease-defining loss in substantia nigra pars compacta (SNpc). The mitochondrion has a particularly important role as cellular "powerhouse" neurons. Therefore, mitochondria become promising therapeutic target treatments. This review aims to describe pathology PD, outline genes factors related summarize current knowledge on quality control give an overview strategies targeting neuroprotective interventions
Language: Английский
Citations
74
Nature Reviews Molecular Cell Biology, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 27, 2025
Language: Английский
Citations
3
Biomedicine & Pharmacotherapy, Journal Year: 2022, Volume and Issue: 149, P. 112890 - 112890
Published: March 31, 2022
In eukaryotic cells, organelles could coordinate complex mechanisms of signaling transduction metabolism and gene expression through their functional interactions. The domain between ER mitochondria, called mitochondria-associated membranes (MAM), is closely associated with various physiological functions including intracellular lipid transport, Ca2+ transfer, mitochondria function maintenance, autophagosome formation. addition, more evidence suggests that MAM modulate cellular in health disease. Studies have also demonstrated the association numerous diseases, neurodegenerative cancer, viral infection, obesity, diabetes. fact, recent revealed a close relationship Alzheimer's disease (AD), Parkinson's (PD), Huntington's (HD), amyotrophic lateral sclerosis (ALS), other diseases. this view, elucidating role diseases particularly important. This review will focus main tethering protein complexes MAM. Besides, regulation potential molecular introduced to provide new understanding pathogenesis these
Language: Английский
Citations
39
Cell Calcium, Journal Year: 2023, Volume and Issue: 112, P. 102743 - 102743
Published: April 25, 2023
Language: Английский
Citations
35
Poultry Science, Journal Year: 2023, Volume and Issue: 102(12), P. 103013 - 103013
Published: Aug. 18, 2023
Vanadium (V) is an essential mineral element in animals, but excessive V can lead to many diseases, affecting the health of humans and animals. However, molecular crosstalk between mitochondria-associated endoplasmic reticulum membranes (MAMs) inflammation under exposure still at exploratory stage. This study was conducted determine MAMs ducks. In this study, duck hepatocytes were treated with NaVO3 (0 μM, 100 200 μM) 2-aminoethyl diphenyl borate (2-APB) (IP3R inhibitor) alone or combination for 24 h. The data showed that exposure-induced cell vacuolization, enlarged intercellular space, decreased density viability. Meanwhile, hydrogen peroxide (H2O2), malonaldehyde (MDA), catalase (CAT), superoxide dismutase (SOD), reactive oxygen species (ROS) levels upregulated treatment. addition, could a marked reduction structure, destruction membrane structure overload intracellular Ca2+ mitochondrial Ca2+. Moreover, treatment resulted notable upregulation MAMs-relevant factors (IP3R, Mfn2, Grp75, MCU, VDAC1) downregulated IL-18, IL-1β, lactate dehydrogenase (LDH) supernatant. Additionally, it also significantly elevated inflammation-relevant (NLRP3, ASC, caspase-1, MAVS, TXNIP). inhibition IP3R expression attenuated V-induced variations above indicators. Collectively, our results revealed maintenance calcium homeostasis protect from injury via MAMs.
Language: Английский
Citations
30
Nutrients, Journal Year: 2023, Volume and Issue: 15(16), P. 3585 - 3585
Published: Aug. 15, 2023
Parkinson’s disease (PD) is a degenerative condition resulting from the loss of dopaminergic neurons. This neuronal leads to motor and non-motor neurological symptoms. Most PD cases are idiopathic, no cure available. Recently, it has been proposed that insulin resistance (IR) could be central factor in development. IR associated with neuropathological features like α-synuclein aggregation, loss, neuroinflammation, mitochondrial dysfunction, autophagy. These related impaired metabolism, death, aggravation Moreover, pharmacological options involve signaling improvement non-dopaminergic strategies have under drugs prevent metabolic pathways involved damage. All these approaches improve outcomes. Also, new biomarker identification may allow for an earlier diagnosis high-risk individuals. review describes main implicated development involving IR. presents several therapeutic directed at used treatment. The understanding molecular mechanisms neurodegenerative enhance diagnosis.
Language: Английский
Citations
29
Current Medical Science, Journal Year: 2022, Volume and Issue: 42(2), P. 237 - 248
Published: April 1, 2022
Abstract Ischemic stroke is a serious cerebrovascular disease with high morbidity and mortality. As result of ischemia-reperfusion, cascade pathophysiological responses triggered by the imbalance in metabolic supply demand, resulting cell loss. These cellular injuries follow various molecular mechanisms solely or combination this disorder. Mitochondria play driving role processes ischemic stroke. Once occurs, damaged cells would respond to such stress through mitophagy. Mitophagy known as conservatively selective autophagy, contributing removal excessive protein aggregates intracellular components, well aging mitochondria. Moderate mitophagy may exert neuroprotection against Several pathways associated mitochondrial network collectively contribute recovering homeostasis neurovascular unit. However, also promote ischemia-reperfusion injury. Therefore, double-edged sword, which suggests that maximizing benefits one direction future efforts. This review emphasized stroke, highlighted crosstalk between apoptosis/necroptosis.
Language: Английский
Citations
33
Neurotoxicity Research, Journal Year: 2023, Volume and Issue: 41(6), P. 708 - 729
Published: May 10, 2023
Language: Английский
Citations
20