BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS生物化学与生物物理学报-脂质的分子与细胞生物学
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS(英文缩写 BBA-MOL CELL BIOL L),ISSN 1388-1981,eISSN 1879-2618,中文译名:生物化学与生物物理学报-脂质的分子与细胞生物学 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-28 至 2026-09-28，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 5.228 | Q1 |
| 2022 | 4.800 | Q1 |
| 2023 | 3.900 | Q1 |
| 2024 | 3.300 | Q2 |
| 2025 | 3.800 | Q1 |
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS 最新收录文献
-
1. Lipidomic and transcriptomic reveals glycerophospholipid and sphingolipid disorders in CVB3 induced viral myocarditis.
PMID:日期:2026-10-01Lipids, which possess a variety of physiological functions, have been demonstrated to be involved in the development of CVB3-induced viral myocarditis (VM). Nevertheless, the dynamic changes of lipid in VM, along with the underlying mechanisms, still require clarification. In our study, the serum and heart lipidomics in both the NC and VM groups was performed by LC-MS/MS. Univariate and multivariate statistical analyses were employed to identify the differential lipids between groups. The heart samples were further tested by the transcriptomic analysis to find the expression profile changes of genes involved in lipid metabolism. Totally, 628 differential lipids in the heart and 666 in the serum were selected based on the criteria of VIP > 1.0, P < 0.05, and fold change >1 or < 1, respectively. Glycerophospholipids (GP) and sphingolipids (SP) were identified as the primary differential lipids, suggesting a marked imbalance in the corresponding lipid metabolic pathways that may be involved in the progression of VM. Simultaneously, the transcriptional profile proved that differentially expressed genes (DEGs) were significantly enriched in GP and SP metabolism pathways. In the serum, the GP category members DLCL (20:5/22:6) and CL (23:1/18:0/22:4/22:6), as well as the SP category members Hex2Cer (d18:2/24:0) and SPHP (d20:1), exhibited a two-fold change. Collectively, combined with transcriptomics and lipidomics data suggest that CVB3 exert its destructive effect on heart possibly by regulating GP and SP metabolism pathways. Several lipids in serum may serve as potential indicators for the progression of VM.
-
2. Diverse methyl-end desaturases enable LC-PUFA biosynthesis across Annelida.
PMID:日期:2026-10-01Recent studies have demonstrated that annelids possess front-end desaturases and elongases involved in the biosynthesis of physiologically important long-chain polyunsaturated fatty acids (LC-PUFA). However, methyl-end desaturases (ωx desaturases), enzymes that play a central role in the de novo biosynthesis of polyunsaturated fatty acids and their subsequent conversion into LC-PUFA, have so far been reported in only a limited number of polychaete species. To advance our understanding of ωx desaturases across the phylum Annelida, this study performed a comprehensive molecular and functional characterisation of these enzymes in the major annelid taxa Polychaeta, Clitellata and Sipuncula, encompassing species from diverse taxonomic groups and ecological niches. A total of 110 ωx desaturase sequences were retrieved from available genomes and transcriptomes. The number of ωx desaturase genes varied among species, ranging from zero to four copies. Phylogenetic analyses revealed that annelid ωx desaturases are classified into two major clades, designated Cluster A and Cluster B. Analyses of histidine-box motifs and exon-intron organisation revealed conserved patterns within each clade. Functional characterisation of ωx desaturases from Eisenia fetida (Clitellata) and Sipunculus nudus (Sipuncula), together with previously published data from polychaetes, demonstrated that annelids generally possess two ωx desaturases, one with Δ12 desaturase activity and another with ω3 desaturase activity. Collectively, these results demonstrate that annelids possess a phylogenetically and functionally diverse ωx desaturase repertoire that underpins their LC-PUFA biosynthetic capacity and may reflect adaptation to different ecological and nutritional environments.
-
3. Fructooligosaccharides ameliorate hepatic and renal lipid accumulation and intestinal barrier dysfunctions in a pre-diabetic rat model.
3. 低聚果糖改善糖尿病前期大鼠模型中的肝肾脂质积聚和肠屏障功能障碍PMID:日期:2026-10-01Consumption of a high-fat diet (HFD) diet is a factor associated with several diseases including obesity and its associated complications, especially liver and kidney dysfunction via promoting derangement of lipid metabolism. It has been reported that fructooligosaccharides (FOS) improve insulin sensitivity and ectopic lipid accumulation. The aim of this study was to investigate the effects of FOS on insulin resistance, liver and renal lipid accumulation, inflammasome formation, oxidative stress and intestinal barrier integrity in an obese rat model. Male Wistar rats were fed a normal (ND) or HFD for 16 weeks. The rats given a HFD were then given FOS at 1 or 2 g/day and metformin at 30 mg/kg/day daily for 8 weeks by oral gavage. The results demonstrated that FOS and metformin improved insulin resistance. FOS showed greater efficacy than metformin in attenuating intestinal barrier leakage. FOS and metformin decreased liver lipid synthesis as evidenced by the downregulation of SREBP1c, FAS and perilipin2. Renal lipid accumulation was restored concomitant with the reduction in renal lipid content and lipotoxicity. Liver and renal inflammation and organ injury were restored to within normal limits. However, FOS had no effect on the antioxidant enzymes via KEAP1/NRF2. Metformin attenuated renal oxidative stress via the suppression of PKCα and the FOXO1 signaling pathway. These suggest that FOS and metformin have the potential to improve gut health and prevent liver and renal complications and could be used as a useful supplement in the obese condition.
-
4. YAP/TAZ knockdown reduces lipid droplet accumulation in hepatic cells through a putative SBDSP1/miR-29a-5p/LDLR regulatory axis.
PMID:日期:2026-10-01Yes-associated protein (YAP) and transcriptional co-activator with PDZ-binding motif (TAZ) are central downstream effectors of the Hippo pathway and play key roles in hepatic metabolic regulation. However, the molecular mechanisms by which YAP/TAZ modulate lipid processing in hepatocytes remain incompletely understood. In this study, we investigated a YAP/TAZ-dependent non-coding RNA regulatory network controlling low-density lipoprotein receptor (LDLR) expression and lipid droplet accumulation in human hepatic cells. Using transcriptomic profiling combined with functional validation in human hepatocellular carcinoma cells, we identified the long non-coding RNA Shwachman-Bodian-Diamond Syndrome Pseudogene 1 (SBDSP1) as a YAP/TAZ-downstream transcript that positively regulates LDLR expression. Silencing of YAP/TAZ significantly reduced SBDSP1 levels, accompanied by downregulation of LDLR mRNA and protein, impaired LDL uptake, and reduced intracellular lipid droplet accumulation. Mechanistically, SBDSP1 was predicted to interact with miR-29a-5p, a microRNA putatively targeting the 3' untranslated region of LDLR. Knockdown of SBDSP1 or mimicking of miR-29a-5p decreased LDLR expression and reduced lipid accumulation, while luciferase reporter assays confirmed direct interactions between miR-29a-5p and both SBDSP1 and LDLR. Collectively, these findings describe a potential YAP/TAZ-SBDSP1-miR-29a-5p-LDLR regulatory axis that controls hepatic lipid uptake and accumulation. This study provides molecular insights into the interplay between Hippo pathway signaling and non-coding RNA networks to regulate lipid metabolism, highlighting a potential regulatory mechanism that may be relevant to hepatic lipid accumulation in metabolic dysfunction-associated steatotic liver disease.
-
5. Moderate-altitude hypoxia is associated with attenuated diet-induced liver injury and coordinated carbon-metabolic and lipid remodeling.
PMID:日期:2026-10-01Chronic mild hypoxia at moderate altitude (2260 m) has been linked to improved systemic metabolism, but its liver-specific associations under high-energy diets remain incompletely defined. In this study, age-matched male C57BL/6 J mice were maintained for 15 weeks at simulated low altitude (50 m) or moderate altitude (2260 m) while fed a normal diet (ND), high-fat diet (HFD), or HFD with 30% fructose (HFD + HFr). Hepatic outcomes were assessed using ultrasonography, histology, electron microscopy, serum biochemistry, targeted energy metabolomics, lipidomics, and immunoblotting. Compared with the corresponding low-altitude high-energy diet groups, mice at 2260 m showed lower diet-associated weight gain, hepatic steatosis, and ALT/AST elevations. Structural analyses showed reduced lipid-droplet accumulation and qualitatively improved mitochondrial ultrastructural appearance. Metabolomics showed coordinated decreases in steady-state intermediates across glycolysis, the pentose phosphate pathway, and the tricarboxylic acid cycle relative to the 50 m HFD group, together with enzyme changes consistent with reduced lipogenic capacity and altered fatty-acid uptake/oxidation. Lipidomic profiling further showed lower accumulation of neutral lipids, including triglycerides and diacylglycerols, as well as sphingolipids, while phospholipid class-level composition appeared less disturbed. Overall, moderate-altitude exposure was associated with attenuation of high-energy-diet-related hepatic metabolic dysfunction and with coordinated metabolic remodeling. These findings identify chronic mild hypoxia as an important contextual factor associated with hepatic metabolic responses, while direct causal mechanisms require further validation.
-
6. HCV clearance by direct-acting antivirals reduces serum phosphatidylethanolamine and improves phospholipid balance.
PMID:日期:2026-09-24Phosphatidylethanolamine (PE) contributes to hepatitis C virus (HCV) replication. Although direct-acting antivirals (DAAs) achieve rapid viral clearance and normalize circulating lipid abnormalities, their effects on the serum PE profile remain incompletely defined. We longitudinally investigated 18 serum PE species during DAA therapy in 178 patients with chronic HCV infection. PE species were quantified using direct-flow injection tandem mass spectrometry on a triple-quadrupole platform. Samples were collected before treatment and at weeks 4 and 12 of DAA therapy. DAA therapy was associated with declines in PE 36:4, PE 38:4, 38:6, 40:5, and 40:6, as well as total serum PE. In parallel, the serum phosphatidylcholine-to-phosphatidylethanolamine (PC/PE) ratio increased. Most PE species, total PE levels, and the PC/PE ratio did not correlate with routine laboratory markers of liver disease or with the Model for End-Stage Liver Disease score. Consistent with this, total PE levels and the PC/PE ratio were similar in patients with and without cirrhosis at the end of treatment. However, cirrhosis was associated with higher PE 36:3 and lower PE 38:4, 38:6, and 40:6. Patients infected with HCV genotype 3a had lower levels of eight PE species and lower total PE, whereas the PC/PE ratio was unchanged. These genotype-associated differences were no longer evident by the end of therapy. In summary, HCV clearance with DAA therapy is associated with marked remodeling of the serum PE profile, characterized by lower total PE levels and an improved PC/PE ratio. These findings suggest circulating phospholipid levels approaching normal after viral eradication.
-
7. ApoE deficiency in mice exacerbates antigen-induced arthritis, alters HDL anti-oxidant capacity and promotes macrophage activation which are reversed by simvastatin treatment.
PMID:日期:2026-09-19Rheumatoid arthritis (RA) is characterized by inflammation and an increased risk for cardiovascular disease. Although it is known that metabolic disturbances alter macrophage metabolism, inflammatory responses and the ability to maintain immune homeostasis, these changes have not been well studied out of the context of atherosclerosis. Our aim was to investigate the effect of dyslipidemia caused by ApoE deficiency on macrophages and on antigen-induced arthritis in mice. Toward this aim, mice deficient in the ApoE gene were used which exhibit high total cholesterol (TC) levels distributed primarily in VLDL/IDL fractions, normal triglycerides and low HDL-C levels associated with distribution at lower densities and lower PON-1 activity. ApoE KO peritoneal macrophages had an M1-like polarization and an increased respiration rate. Importantly, ApoE KO mice developed more severe knee joint swelling compared to control mice. At the end of the arthritis protocol, spleen macrophages had increased expression of M1 cell surface markers. Simvastatin treatment reduced serum TC, increased HDL-C and PON-1 activity and improved HDL density. Additionally, treatment of ApoE KO mice with simvastatin limited the M1-associated cell surface markers on spleen macrophages and reduced arthritic joint swelling. Collectively, our findings support further investigation of lipid-modifying strategies in the context of inflammatory arthritis associated with dyslipidemia.
-
8. {"_":"Retinoic acid-inducible prostaglandin I receptor is required for the development of proximal tubules in zebrafish.","sub":["2"]}
PMID:日期:2026-09-15The nephron comprises specialized segments, such as the glomerulus and tubules, and is the structural and functional unit of the kidney. Nephron formation in development is important for subsequent normal nephric function. However, mechanisms regulating the nephron segment formation (nephron segmentation) remain unclear. Here, we report that the prostaglandin (PG) I-IP receptor is required for the development of proximal tubules in zebrafish. We identified expression of the IP receptor in the proximal tubules during nephron segmentation. This expression was abolished by an inhibitor of retinoic acid (RA) synthases and antagonists of RA nuclear receptors. The loss of IP receptor expression induced by the RA synthase inhibitor was restored by the addition of RA. These results suggest that RA induces IP receptor expression in the proximal tubules during nephron segmentation through RA nuclear receptors. Intriguingly, knockout of the IP receptor caused impaired differentiation into proximal tubule cells and nephric multiciliated cells, an aberrant balance between proximal and distal tubules, and abnormal kidney function, which are similar to the phenomena observed by inhibition of RA signaling during nephron segmentation. Consistently, inhibition of PG synthesis by an inhibitor of PG synthases caused impaired differentiation into proximal tubule cells and nephric multiciliated cells and the aberrant balance between proximal and distal tubules. These impairments and the aberrant balance between the tubules were restored by the addition of an IP receptor agonist. Therefore, these findings highlight that the PGI-IP receptor plays a crucial role in nephron segmentation downstream of RA signaling in proximal tubules.
-
9. Astaxanthin attenuates pro-inflammatory signaling and promotes adipogenesis in human adipose stem cells.
PMID:日期:2026-08-31Adipose tissues not only store and release energy but also function as endocrine organs and maintaining adipose stem cells (ASCs) and functional adipocytes is essential for systemic metabolic health. Astaxanthin (Ast), an oxygenated carotenoid enriched in seafood, is recognized as a bioactive compound known for its anti-inflammatory and antioxidative properties. However, limited information is available regarding the roles of Ast in human ASCs (hASCs). This study examined the capacity of Ast to counteract TNF-α actions in the inflammatory signaling pathways and proliferation of hASCs. The effects of Ast on hASC adipogenesis and the underlying mechanisms were also determined. Proliferation rates were measured with an MTT assay, and adipogenesis was determined by measuring the expression levels of adipogenic markers and lipid accumulation. Ast (0.01-10 μM) had no effect under basal conditions but attenuated TNFα-mediated suppression of cell viability, as well as activation of canonical proinflammatory signaling pathways in hASCs. Lower concentrations of Ast (0.01 and 0.1 μM) increased adipogenesis, while higher concentrations (2 and 10 μM) inhibited adipogenesis. Ast (0.01 and 0.1 μM) induced adipogenesis by suppressing the anti-adipogenic Wnt/β-catenin pathway and upregulating the adipogenic transcription factors, C/EBPα and PPARγ, during the early periods of adipogenesis. Our results suggest that Ast has beneficial impacts on adipose tissue by suppressing inflammation, thereby maintaining the pool of adipose progenitors and promoting their adipogenesis.
-
10. Attenuation of liver fibrosis by platelet-type 12S-lipoxygenase expressed in hepatic stellate cells involves repression of platelet-derived growth factor receptors.
PMID:日期:2026-08-27Progression of liver fibrosis is a critical determinant of the prognosis of chronic inflammatory liver disease. We previously reported that platelet-type 12S-lipoxygenase localized in hepatic stellate cells (HSCs), which are primary fibrogenic cells in the injured liver, was upregulated in a methionine-choline deficiency (MCD) diet-induced mouse liver fibrosis model. In this study, the functional contribution of platelet-type 12S-lipoxygenase to the pathological process was investigated. After feeding with an MCD diet for 8 weeks, platelet-type 12S-lipoxygenase-deficient (Alox12) mice exhibited significantly greater Sirius Red-positive areas and higher expression of type I collagen genes (Col1a1 and Col1a2) than wild-type (WT) mice, indicating aggravated fibrosis. Similar results were obtained in a model induced by neonatal streptozotocin injection followed by a high-fat diet (HFD) feeding. Conversely, a human HSC line (TWNT-1) stably overexpressing human platelet-type 12S-lipoxygenase exhibited significantly reduced COL1A1 and COL1A2 expression compared to the parental and mock cells. Analysis of fibrosis-related genes revealed downregulation of platelet-derived growth factor receptors (PDGFR) α and β in platelet-type 12S-lipoxygenase-expressing TWNT-1 cells. Consistently, the hepatic expression of Pdgfra and Pdgfrb was significantly elevated in MCD diet-fed Alox12 mice compared to that in MCD diet-fed WT mice. The knockdown of PDGFRs in parental TWNT-1 cells using siRNAs significantly suppressed the expression of type I collagen genes. Collectively, these findings indicate that platelet-type 12S-lipoxygenase expressed in HSCs attenuates liver fibrosis, at least in part, by modulating PDGFR expression.