Exploring the role of Prx II in mitigating endoplasmic reticulum stress and mitochondrial dysfunction in neurodegeneration
Neurodegenerative diseases are increasingly recognized for their association with oxidative stress, which leads to progressive dysfunction and loss of neurons, manifesting in cognitive and motor impairments. T... (Source: Cell Communication and Signaling)
Source: Cell Communication and Signaling - April 18, 2024 Category: Molecular Biology Authors: Mei-Hua Jin, Lin Feng, Hong-Yi Xiang, Hu-Nan Sun, Ying-Hao Han and Taeho Kwon Tags: Research Source Type: research
Molecules, Vol. 29, Pages 1848: Advanced Nano-Drug Delivery Systems in the Treatment of Ischemic Stroke
Chen
In recent years, the frequency of strokes has been on the rise year by year and has become the second leading cause of death around the world, which is characterized by a high mortality rate, high recurrence rate, and high disability rate. Ischemic strokes account for a large percentage of strokes. A reperfusion injury in ischemic strokes is a complex cascade of oxidative stress, neuroinflammation, immune infiltration, and mitochondrial damage. Conventional treatments are ineffective, and the presence of the blood–brain barrier (BBB) leads to inefficient drug delivery utilization, so researchers are...
Source: Molecules - April 18, 2024 Category: Chemistry Authors: Jiajie Zhang Zhong Chen Qi Chen Tags: Review Source Type: research
Mini-encyclopedia of mitochondria-relevant nutraceuticals protecting health in primary and secondary care —clinically relevant 3PM innovation
AbstractDespite their subordination in humans, to a great extent, mitochondria maintain their independent status but tightly cooperate with the “host” on protecting the joint life quality and minimizing health risks. Under oxidative stress conditions, healthy mitochondria promptly increase mitophagy level to remove damaged “fellows” rejuvenating the mitochondrial population and sending fragments of mtDNA as SOS signals to all system s in the human body. As long as metabolic pathways are under systemic control and well-concerted together, adaptive mechanisms become triggered increasing systemic protection, activatin...
Source: EPMA Journal - April 18, 2024 Category: International Medicine & Public Health Source Type: research
FoxG1 as a Potential Therapeutic Target for Alzheimer's Disease: Modulating NLRP3 Inflammasome via AMPK/mTOR Autophagy Pathway
Cell Mol Neurobiol. 2024 Apr 17;44(1):35. doi: 10.1007/s10571-024-01467-4.ABSTRACTAn increasing body of research suggests that promoting microglial autophagy hinders the neuroinflammation initiated though the NLRP3 inflammasome activation in Alzheimer's disease (AD). The function of FoxG1, a crucial transcription factor involved in cell survival by regulating mitochondrial function, remains unknown during the AD process and neuroinflammation occurs. In the present study, we firstly found that Aβ peptides induced AD-like neuroinflammation upregulation and downregulated the level of autophagy. Following low-dose Aβ25-35 st...
Source: Cellular and Molecular Neurobiology - April 17, 2024 Category: Cytology Authors: Qi Yun Si-Fei Ma Wei-Ning Zhang Meng Gu Jia Wang Source Type: research
Calorie restriction anti-hypertrophic effects are associated with improved mitochondrial content, blockage of Ca < sup > 2+ < /sup > -induced mitochondrial damage, and lower reverse electron transport-mediated oxidative stress
In this study, we show that this dietetic intervention prevents cardiac protein elevation, avoids fetal gene reprogramming (atrial natriuretic peptide), and blocks the increase in heart weight per tibia length index (HW/TL) seen in isoproterenol-induced cardiac hypertrophy. Our findings suggest that calorie restriction inhibits cardiac pathological growth while also lowering mitochondrial reverse electron transport-induced hydrogen peroxide formation and improving mitochondrial content. Calorie restriction also attenuated the opening of the Ca2+-induced mitochondrial permeability transition pore. We also found that calorie...
Source: Free Radical Research - April 17, 2024 Category: Research Authors: Aline Maria Brito Lucas Plinio Bezerra Palacio Pedro Lourenzo Oliveira Cunha Heberty Tarso Facundo Source Type: research
Triclocarban induces lipid droplet accumulation and oxidative stress responses by inhibiting mitochondrial fatty acid oxidation in HepaRG cells
Toxicol Lett. 2024 Apr 15:S0378-4274(24)00067-5. doi: 10.1016/j.toxlet.2024.04.002. Online ahead of print.ABSTRACTMitochondrial fatty acid oxidation (mtFAO) plays an important role in hepatic energy metabolism. Severe mtFAO injury leads to nonalcoholic fatty liver disease (NAFLD) and liver failure. Several drugs have been withdrawn owing to safety issues, such as induction of fatty liver disease through mtFAO disruption. For instance, the antimicrobial triclocarban (TCC), an environmental contaminant that was removed from the market due to its unknown safety in humans, induces NAFLD in rats and promotes hepatic FAO in mice...
Source: Toxicology Letters - April 17, 2024 Category: Toxicology Authors: Hitoshi Nakamura Toshikatsu Matsui Tadahiro Shinozawa Source Type: research
The paradox of fatty-acid β-oxidation in muscle insulin resistance: Metabolic control and muscle heterogeneity
Biochim Biophys Acta Mol Basis Dis. 2024 Apr 15:167172. doi: 10.1016/j.bbadis.2024.167172. Online ahead of print.ABSTRACTThe skeletal muscle is a metabolically heterogeneous tissue that plays a key role in maintaining whole-body glucose homeostasis. It is well known that muscle insulin resistance (IR) precedes the development of type 2 diabetes. There is a consensus that the accumulation of specific lipid species in the tissue can drive IR. However, the role of the mitochondrial fatty-acid β-oxidation in IR and, consequently, in the control of glucose uptake remains paradoxical: interventions that either inhibit or activa...
Source: Biochimica et Biophysica Acta - April 17, 2024 Category: Biochemistry Authors: Marcel A Vieira-Lara Barbara M Bakker Source Type: research
Mitochondrial calcium signaling in non-neuronal cells: Implications for Alzheimer's disease pathogenesis
Biochim Biophys Acta Mol Basis Dis. 2024 Apr 15:167169. doi: 10.1016/j.bbadis.2024.167169. Online ahead of print.ABSTRACTMitochondrial dysregulation is pivotal in Alzheimer's disease (AD) pathogenesis. Calcium governs vital mitochondrial processes impacting energy conversion, oxidative stress, and cell death signaling. Disruptions in mitochondrial calcium (mCa2+) handling induce calcium overload and trigger the opening of mitochondrial permeability transition pore, ensuing energy deprivation and resulting in AD-related neuronal cell death. However, the role of mCa2+ in non-neuronal cells (microglia, astrocytes, oligodendro...
Source: Biochimica et Biophysica Acta - April 17, 2024 Category: Biochemistry Authors: Darpan Raghav Shatakshi Shukla Pooja Jadiya Source Type: research
FoxG1 as a Potential Therapeutic Target for Alzheimer's Disease: Modulating NLRP3 Inflammasome via AMPK/mTOR Autophagy Pathway
Cell Mol Neurobiol. 2024 Apr 17;44(1):35. doi: 10.1007/s10571-024-01467-4.ABSTRACTAn increasing body of research suggests that promoting microglial autophagy hinders the neuroinflammation initiated though the NLRP3 inflammasome activation in Alzheimer's disease (AD). The function of FoxG1, a crucial transcription factor involved in cell survival by regulating mitochondrial function, remains unknown during the AD process and neuroinflammation occurs. In the present study, we firstly found that Aβ peptides induced AD-like neuroinflammation upregulation and downregulated the level of autophagy. Following low-dose Aβ25-35 st...
Source: Cellular and Molecular Neurobiology - April 17, 2024 Category: Cytology Authors: Qi Yun Si-Fei Ma Wei-Ning Zhang Meng Gu Jia Wang Source Type: research
Calorie restriction anti-hypertrophic effects are associated with improved mitochondrial content, blockage of Ca < sup > 2+ < /sup > -induced mitochondrial damage, and lower reverse electron transport-mediated oxidative stress
In this study, we show that this dietetic intervention prevents cardiac protein elevation, avoids fetal gene reprogramming (atrial natriuretic peptide), and blocks the increase in heart weight per tibia length index (HW/TL) seen in isoproterenol-induced cardiac hypertrophy. Our findings suggest that calorie restriction inhibits cardiac pathological growth while also lowering mitochondrial reverse electron transport-induced hydrogen peroxide formation and improving mitochondrial content. Calorie restriction also attenuated the opening of the Ca2+-induced mitochondrial permeability transition pore. We also found that calorie...
Source: Free Radical Research - April 17, 2024 Category: Research Authors: Aline Maria Brito Lucas Plinio Bezerra Palacio Pedro Lourenzo Oliveira Cunha Heberty Tarso Facundo Source Type: research
Mitochondrial calcium signaling in non-neuronal cells: Implications for Alzheimer's disease pathogenesis
Biochim Biophys Acta Mol Basis Dis. 2024 Apr 15;1870(5):167169. doi: 10.1016/j.bbadis.2024.167169. Online ahead of print.ABSTRACTMitochondrial dysregulation is pivotal in Alzheimer's disease (AD) pathogenesis. Calcium governs vital mitochondrial processes impacting energy conversion, oxidative stress, and cell death signaling. Disruptions in mitochondrial calcium (mCa2+) handling induce calcium overload and trigger the opening of mitochondrial permeability transition pore, ensuing energy deprivation and resulting in AD-related neuronal cell death. However, the role of mCa2+ in non-neuronal cells (microglia, astrocytes, oli...
Source: Biochimica et Biophysica Acta - April 17, 2024 Category: Biochemistry Authors: Darpan Raghav Shatakshi Shukla Pooja Jadiya Source Type: research
The paradox of fatty-acid β-oxidation in muscle insulin resistance: Metabolic control and muscle heterogeneity
Biochim Biophys Acta Mol Basis Dis. 2024 Apr 15:167172. doi: 10.1016/j.bbadis.2024.167172. Online ahead of print.ABSTRACTThe skeletal muscle is a metabolically heterogeneous tissue that plays a key role in maintaining whole-body glucose homeostasis. It is well known that muscle insulin resistance (IR) precedes the development of type 2 diabetes. There is a consensus that the accumulation of specific lipid species in the tissue can drive IR. However, the role of the mitochondrial fatty-acid β-oxidation in IR and, consequently, in the control of glucose uptake remains paradoxical: interventions that either inhibit or activa...
Source: Biochimica et Biophysica Acta - April 17, 2024 Category: Biochemistry Authors: Marcel A Vieira-Lara Barbara M Bakker Source Type: research
Triclocarban induces lipid droplet accumulation and oxidative stress responses by inhibiting mitochondrial fatty acid oxidation in HepaRG cells
Toxicol Lett. 2024 Apr 15;396:11-18. doi: 10.1016/j.toxlet.2024.04.002. Online ahead of print.ABSTRACTMitochondrial fatty acid oxidation (mtFAO) plays an important role in hepatic energy metabolism. Severe mtFAO injury leads to nonalcoholic fatty liver disease (NAFLD) and liver failure. Several drugs have been withdrawn owing to safety issues, such as induction of fatty liver disease through mtFAO disruption. For instance, the antimicrobial triclocarban (TCC), an environmental contaminant that was removed from the market due to its unknown safety in humans, induces NAFLD in rats and promotes hepatic FAO in mice. Therefore,...
Source: Toxicology Letters - April 17, 2024 Category: Toxicology Authors: Hitoshi Nakamura Toshikatsu Matsui Tadahiro Shinozawa Source Type: research
Calorie restriction anti-hypertrophic effects are associated with improved mitochondrial content, blockage of Ca < sup > 2+ < /sup > -induced mitochondrial damage, and lower reverse electron transport-mediated oxidative stress
In this study, we show that this dietetic intervention prevents cardiac protein elevation, avoids fetal gene reprogramming (atrial natriuretic peptide), and blocks the increase in heart weight per tibia length index (HW/TL) seen in isoproterenol-induced cardiac hypertrophy. Our findings suggest that calorie restriction inhibits cardiac pathological growth while also lowering mitochondrial reverse electron transport-induced hydrogen peroxide formation and improving mitochondrial content. Calorie restriction also attenuated the opening of the Ca2+-induced mitochondrial permeability transition pore. We also found that calorie...
Source: Free Radical Research - April 17, 2024 Category: Research Authors: Aline Maria Brito Lucas Plinio Bezerra Palacio Pedro Lourenzo Oliveira Cunha Heberty Tarso Facundo Source Type: research
