
Marine Drugs, Journal Year: 2024, Volume and Issue: 22(11), P. 509 - 509
Published: Nov. 10, 2024
Lipid extracts from the microalgae
Language: Английский
Marine Drugs, Journal Year: 2024, Volume and Issue: 22(11), P. 509 - 509
Published: Nov. 10, 2024
Lipid extracts from the microalgae
Language: Английский
International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(2), P. 788 - 788
Published: Jan. 18, 2025
Diets rich in carbohydrate and saturated fat contents, when combined with a sedentary lifestyle, contribute to the development of obesity metabolic syndrome (MetS), which subsequently increase palmitic acid (PA) levels. At high concentrations, PA induces lipotoxicity through several mechanisms involving endoplasmic reticulum (ER) stress, mitochondrial dysfunction, inflammation cell death. Nevertheless, there are endogenous strategies mitigate PA-induced its unsaturation elongation channeling storage lipid droplets (LDs), plays crucial role sequestering oxidized lipids, thereby reducing oxidative damage membranes. While extended exposure promotes reactive oxygen species (ROS) generation leading damage, acute ß-cells increases glucose-stimulated insulin secretion (GSIS), activation free fatty receptors (FFARs). Subsequently, FFARs by exogenous agonists has been suggested as potential therapeutic strategy prevent ß cells. Moreover, some acids, including oleic acid, can counteract negative impact on cellular health, suggesting complex interaction between different dietary fats outcomes. Therefore, challenge is peroxidation unsaturated acids utilization natural antioxidants. This complexity indicates necessity for further research into function diverse pathological conditions find main target against lipotoxicity. The aim this review is, therefore, examine recent data regarding mechanism underlying order identify that promote protection lipotoxicity, dysfunction apoptosis MetS obesity.
Language: Английский
Citations
3Trends in Biochemical Sciences, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
The majority of eukaryotic proteins undergo N-terminal (Nt) modifications facilitated by various enzymes. These enzymes, which target the initial amino acid a polypeptide in sequence-dependent manner, encompass peptidases, transferases, cysteine oxygenases, and ligases. Nt - such as acetylation, fatty acylations, methylation, arginylation, oxidation enhance proteome complexity regulate protein targeting, stability, complex formation. Modifications at N termini are thereby core components large number biological processes, including cell signaling motility, autophagy regulation, plant animal oxygen sensing. Dysregulation Nt-modifying enzymes is implicated several human diseases. In this feature review we provide an overview occurring either co- or post-translationally, involved, impact.
Language: Английский
Citations
2Journal of Molecular and Cellular Cardiology, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
Language: Английский
Citations
1Nature Communications, Journal Year: 2025, Volume and Issue: 16(1)
Published: Jan. 14, 2025
Language: Английский
Citations
1Journal of Biomedical Science, Journal Year: 2025, Volume and Issue: 32(1)
Published: Feb. 12, 2025
Diabetic neuropathy (DN) is a prevalent and painful complication of diabetes; however, the mechanisms underlying its pathogenesis remain unclear, effective clinical treatments are lacking. This study aims to explore role peroxisomes in Schwann cells DN. The abundance sciatic nerves mice or was analyzed using laser confocal super-resolution imaging western blotting. RFP-GFP-SKL (Ser-Lys-Leu) probe utilized assess pexophagy (peroxisomes autophagy) levels. To evaluate palmitoylation PEX11B, acyl-resin assisted capture (acyl-RAC) assay Acyl-Biotin Exchange (ABE) were employed. Additionally, MR (Mendelian randomization) analysis conducted investigate potential causal relationship between DN MS (Multiple sclerosis). There decrease peroxisomal diabetic mice, palmitic acid (PA) induced reduction by inhibiting biogenesis cells. Mechanistically, PA PEX11B at C25 site, disrupting self-interaction impeding peroxisome elongation. Fenofibrate, PPARα agonist, effectively rescued dysfunction caused restored mice. Lastly, indicates notable influence on MS, with onset progression intricately linked dysfunction. Targeting pathway may be an strategy for preventing treating DN, underscoring importance addressing risk
Language: Английский
Citations
1International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 291, P. 139067 - 139067
Published: Dec. 25, 2024
Language: Английский
Citations
7Cancer Letters, Journal Year: 2024, Volume and Issue: 598, P. 217118 - 217118
Published: July 14, 2024
Language: Английский
Citations
5Frontiers in Nutrition, Journal Year: 2024, Volume and Issue: 11
Published: Sept. 4, 2024
Patients with cancer frequently exhibit alterations in serum lipid profiles associated chemotherapy. It has been reported that distribution correlates tumor progression. However, the prognostic value of biomarkers survivors remains a subject debate. We aim to explore relationship between non-high-density lipoprotein high-density ratio (NHHR) and prognosis survivors.
Language: Английский
Citations
4Journal of Agricultural and Food Chemistry, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 3, 2025
Conjugated linoleic acid (CLA) is known for antiobesity. However, the role of CLA in regulating high-fat diet (HFD)-impaired pubertal mammary gland development remains undefined. Here, female mice and HC11 cells were treated with HFD or palmitic (PA), supplemented without CLA, respectively. We found that prevented impaired exposed to HFD. In vitro, c9, t11-CLA, but not t10, c12-CLA, promoted PA-suppressed proliferation, accompanied by hindered CD36 palmitoylation localization on plasma membrane. Moreover, t11-CLA reduced formation CD36/Fyn/Lyn complex inhibited JNK pathway while activated ERK PA-treated HC11. mechanism, activation inhibition abolished t11-CLA-stimulated proliferation vivo verification, total cell membrane palmitoylation, suppressed CD36/FYN/LYN complex, HFD-fed mice. conclusion, mitigated HFD-impaired via downstream JNK–ERK pathway. These data suggested potential application ameliorating obesity-impaired development.
Language: Английский
Citations
0Trends in Pharmacological Sciences, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
Language: Английский
Citations
0