Journal of Lipid Research最新文献_第10页

ANGPTL8 deficiency attenuates lipopolysaccharide-induced liver injury by improving lipid metabolic dysregulation. ANGPTL8 缺乏症可通过改善脂质代谢失调减轻脂多糖诱导的肝损伤。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-07-15 DOI: 10.1016/j.jlr.2024.100595

Ying Feng, Shan Luo, Chen Fang, Shinan Ma, Dandan Fan, Yanghui Chen, Zhuo Chen, Xiang Zheng, Yijun Tang, Xiaobei Duan, Xingling Liu, Xuzhi Ruan, Xingrong Guo

{"title":"ANGPTL8 deficiency attenuates lipopolysaccharide-induced liver injury by improving lipid metabolic dysregulation.","authors":"Ying Feng, Shan Luo, Chen Fang, Shinan Ma, Dandan Fan, Yanghui Chen, Zhuo Chen, Xiang Zheng, Yijun Tang, Xiaobei Duan, Xingling Liu, Xuzhi Ruan, Xingrong Guo","doi":"10.1016/j.jlr.2024.100595","DOIUrl":"10.1016/j.jlr.2024.100595","url":null,"abstract":"Liver injury is closely related to poor outcomes in sepsis patients. Current studies indicate that sepsis is accompanied by metabolic disorders, especially those related to lipid metabolism. It is highly important to explore the mechanism of abnormal liver lipid metabolism during sepsis. As a key regulator of glucose and lipid metabolism, angiopoietin-like 8 (ANGPTL8) is involved in the regulation of multiple chronic metabolic diseases. In the present study, severe liver lipid deposition and lipid peroxidation were observed in the early stages of lipopolysaccharide (LPS) induced liver injury. LPS promotes the expression of ANGPTL8 both in vivo and in vitro. Knockout of Angptl8 reduced hepatic lipid accumulation and lipid peroxidation, improved fatty acid oxidation and liver function, and increased the survival rate of septic mice by activating the PGC1α/PPARα pathway. We also found that the expression of ANGPTL8 induced by LPS depends on TNF-α, and that inhibiting the TNF-α pathway reduces LPS-induced hepatic lipid deposition and lipid peroxidation. However, knocking out Angptl8 improved the survival rate of septic mice better than inhibiting the TNF-α pathway. Taken together, the results of our study suggest that ANGPTL8 functions as a novel cytokine in LPS-induced liver injury by suppressing the PGC1α/PPARα signaling pathway. Therefore, targeting ANGPTL8 to improve liver lipid metabolism represents an attractive strategy for the management of sepsis patients.","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100595"},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11364043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141633752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The fate of intracellular S1P regulates lipid droplet turnover and lipotoxicity in pancreatic beta-cells. 细胞内 S1P 的去向调节胰腺β细胞中脂滴的周转和脂毒性。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-06-29 DOI: 10.1016/j.jlr.2024.100587

Yadi Tang, Mariola Majewska, Britta Leß, Ilir Mehmeti, Philipp Wollnitzke, Nina Semleit, Bodo Levkau, Julie D Saba, Gerhild van Echten-Deckert, Ewa Gurgul-Convey

{"title":"The fate of intracellular S1P regulates lipid droplet turnover and lipotoxicity in pancreatic beta-cells.","authors":"Yadi Tang, Mariola Majewska, Britta Leß, Ilir Mehmeti, Philipp Wollnitzke, Nina Semleit, Bodo Levkau, Julie D Saba, Gerhild van Echten-Deckert, Ewa Gurgul-Convey","doi":"10.1016/j.jlr.2024.100587","DOIUrl":"10.1016/j.jlr.2024.100587","url":null,"abstract":"Lipotoxicity has been considered the main cause of pancreatic beta-cell failure during type 2 diabetes development. Lipid droplets (LD) are believed to regulate the beta-cell sensitivity to free fatty acids (FFA), but the underlying molecular mechanisms are largely unclear. Accumulating evidence points, however, to an important role of intracellular sphingosine-1-phosphate (S1P) metabolism in lipotoxicity-mediated disturbances of beta-cell function. In the present study, we compared the effects of an increased irreversible S1P degradation (S1P-lyase, SPL overexpression) with those associated with an enhanced S1P recycling (overexpression of S1P phosphatase 1, SGPP1) on LD formation and lipotoxicity in rat INS1E beta-cells. Interestingly, although both approaches led to a reduced S1P concentration, they had opposite effects on the susceptibility to FFA. Overexpression of SGPP1 prevented FFA-mediated caspase-3 activation by a mechanism involving an enhanced lipid storage capacity and prevention of oxidative stress. In contrast, SPL overexpression limited LD biogenesis, content, and size, while accelerating lipophagy. This was associated with FFA-induced hydrogen peroxide formation, mitochondrial fragmentation, and dysfunction, as well as ER stress. These changes coincided with the upregulation of proapoptotic ceramides but were independent of lipid peroxidation rate. Also in human EndoC-βH1 beta-cells, suppression of SPL with simultaneous overexpression of SGPP1 led to a similar and even more pronounced LD phenotype as that in INS1E-SGPP1 cells. Thus, intracellular S1P turnover significantly regulates LD content and size and influences beta-cell sensitivity to FFA.","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100587"},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11345310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141476781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Guselkumab treatment normalizes the stratum corneum ceramide profile and alleviates barrier dysfunction in psoriasis: results of a randomized controlled trial. 古舍库单抗治疗可使角质层神经酰胺分布正常化并缓解银屑病屏障功能障碍：随机对照试验结果。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-07-09 DOI: 10.1016/j.jlr.2024.100591

Jannik Rousel, Catherine Mergen, Menthe E Bergmans, Lisa J Bruijnincx, Marieke L de Kam, Naomi B Klarenbeek, Tessa Niemeyer-van der Kolk, Martijn B A van Doorn, Joke A Bouwstra, Robert Rissmann

{"title":"Guselkumab treatment normalizes the stratum corneum ceramide profile and alleviates barrier dysfunction in psoriasis: results of a randomized controlled trial.","authors":"Jannik Rousel, Catherine Mergen, Menthe E Bergmans, Lisa J Bruijnincx, Marieke L de Kam, Naomi B Klarenbeek, Tessa Niemeyer-van der Kolk, Martijn B A van Doorn, Joke A Bouwstra, Robert Rissmann","doi":"10.1016/j.jlr.2024.100591","DOIUrl":"10.1016/j.jlr.2024.100591","url":null,"abstract":"The epidermal inflammation associated with psoriasis drives skin barrier perturbations. The skin barrier is primarily located in stratum corneum (SC). Its function depends on the SC lipid matrix of which ceramides constitute important components. Changes in the ceramide profile directly correlate to barrier function. In this study, we characterized the dynamics of the barrier function and ceramide profile of psoriatic skin during anti-Interleukin-23 therapy with guselkumab. We conducted a double-blind, randomized controlled trial in which 26 mild-to-severe plaque psoriasis patients were randomization 3:1-100 mg guselkumab or placebo for 16 weeks and barrier dynamics monitored throughout. Barrier function was measured by trans-epidermal water loss measurements. Untargeted ceramide profiling was performed using liquid chromatography-mass spectrometry after SC was harvested using tape-stripping. The barrier function and ceramide profile of lesional skin normalized to that of controls during treatment with guselkumab, but not placebo. This resulted in significant differences compared to placebo at the end of the treatment. Changes in the lesional ceramide profile during treatment correlated with barrier function and target lesion severity. Nonlesional skin remained similar throughout treatment. Guselkumab therapy restored the skin barrier in psoriasis. Concomitant correlations between skin barrier function, the ceramide profile, and disease severity demonstrate their interdependency.","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100591"},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11342092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141590470","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Highly flexible cell membranes are the key to efficient production of lipophilic compounds. 高度灵活的细胞膜是高效生产亲脂化合物的关键。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-07-17 DOI: 10.1016/j.jlr.2024.100597

Qiyao Zhu, Sijia Wang, Gang Fu, Fengming Guo, Wei Huang, Tengyue Zhang, Huina Dong, Zhaoxia Jin, Dawei Zhang

{"title":"Highly flexible cell membranes are the key to efficient production of lipophilic compounds.","authors":"Qiyao Zhu, Sijia Wang, Gang Fu, Fengming Guo, Wei Huang, Tengyue Zhang, Huina Dong, Zhaoxia Jin, Dawei Zhang","doi":"10.1016/j.jlr.2024.100597","DOIUrl":"10.1016/j.jlr.2024.100597","url":null,"abstract":"Lipophilic compounds have a variety of positive effects on human physiological functions and exhibit good effects in the prevention and treatment of clinical diseases. This has led to significant interest in the technical applications of synthetic biology for the production of lipophilic compounds. However, the strict selective permeability of the cell membrane and the hydrophobic nature of lipophilic compounds pose significant challenges to their production. During fermentation, lipophilic compounds tend to accumulate within cell membrane compartments rather than being secreted extracellularly. The toxic effects of excessive lipophilic compound accumulation can threaten cell viability, while the limited space within the cell membrane restricts further increases in production yield. Consequently, to achieve efficient production of lipophilic compounds, research is increasingly focused on constructing robust and multifunctional microbial cell factories. Utilizing membrane engineering techniques to construct highly flexible cell membranes is considered an effective strategy to break through the upper limit of lipophilic compound production. Currently, there are two main approaches to cell membrane modification: constructing artificial storage compartments for lipophilic compounds and engineering the cell membrane structure to facilitate product outflow. This review summarizes recent cell membrane engineering strategies applied in microbial cell factories for the production of liposoluble compounds, discussing the challenges and future prospects. These strategies enhance membrane flexibility and effectively promote the production of liposoluble compounds.","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100597"},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11367113/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141727222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Peridroplet mitochondria are associated with the severity of MASLD and the prevention of MASLD by diethyldithiocarbamate. 线粒体周围与 MASLD 的严重程度以及二乙基二硫代氨基甲酸盐对 MASLD 的预防有关。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-07-07 DOI: 10.1016/j.jlr.2024.100590

Xiangyun Sun, Qinghong Yu, Yifei Qi, Bilian Kang, Xinyan Zhao, Lin Liu, Ping Wang, Min Cong, Tianhui Liu

{"title":"Peridroplet mitochondria are associated with the severity of MASLD and the prevention of MASLD by diethyldithiocarbamate.","authors":"Xiangyun Sun, Qinghong Yu, Yifei Qi, Bilian Kang, Xinyan Zhao, Lin Liu, Ping Wang, Min Cong, Tianhui Liu","doi":"10.1016/j.jlr.2024.100590","DOIUrl":"10.1016/j.jlr.2024.100590","url":null,"abstract":"Mitochondria can contact lipid droplets (LDs) to form peridroplet mitochondria (PDM) which trap fatty acids in LDs by providing ATP for triglyceride synthesis and prevent lipotoxicity. However, the role of PDM in metabolic dysfunction associated steatotic liver disease (MASLD) is not clear. Here, the features of PDM in dietary MASLD models with different severity in mice were explored. Electron microscope photographs show that LDs and mitochondria rarely come into contact with each other in normal liver. In mice fed with high-fat diet, PDM can be observed in the liver as early as the beginning of steatosis in hepatocytes. For the first time, we show that PDM in mouse liver varies with the severity of MASLD. PDM and cytosolic mitochondria were isolated from the liver tissue of MASLD and analyzed by quantitative proteomics. Compared with cytosolic mitochondria, PDM have enhanced mitochondrial respiration and ATP synthesis. Diethyldithiocarbamate (DDC) alleviates choline-deficient, L-amino acid-defined diet-induced MASLD, while increases PDM in the liver. Similarly, DDC promotes the contact of mitochondria-LDs in steatotic C3A cells in vitro. Meanwhile, DDC promotes triglyceride synthesis and improves mitochondrial dysfunction in MASLD. In addition, DDC upregulates perilipin 5 both in vivo and in vitro, which is considered as a key regulator in PDM formation. Knockout of perilipin 5 inhibits the contact of mitochondria-LDs induced by DDC in C3A cells. These results demonstrate that PDM might be associated with the progression of MASLD and the prevention of MASLD by DDC.","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100590"},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11381863/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141563543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

All-trans retinoic acid induces lipophagy by reducing Rubicon in Hepa1c1c7 cells. 全反式维甲酸通过减少 Hepa1c1c7 细胞中的 Rubicon 来诱导脂肪吞噬。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-07-18 DOI: 10.1016/j.jlr.2024.100598

Anh The Nguyen, Masashi Masuda, Yuki Mori, Yuichiro Adachi, Teppei Fukuda, Airi Furuichi, Masaki Takikawa, Yuki Tsuda, Yuki Hamada, Yusuke Maruyama, Hirokazu Ohminami, Kohta Ohnishi, Yutaka Taketani

{"title":"All-trans retinoic acid induces lipophagy by reducing Rubicon in Hepa1c1c7 cells.","authors":"Anh The Nguyen, Masashi Masuda, Yuki Mori, Yuichiro Adachi, Teppei Fukuda, Airi Furuichi, Masaki Takikawa, Yuki Tsuda, Yuki Hamada, Yusuke Maruyama, Hirokazu Ohminami, Kohta Ohnishi, Yutaka Taketani","doi":"10.1016/j.jlr.2024.100598","DOIUrl":"10.1016/j.jlr.2024.100598","url":null,"abstract":"All-trans retinoic acid (atRA), a metabolite of vitamin A, reduces hepatic lipid accumulation in liver steatosis model animals. Lipophagy, a new lipolysis pathway, degrades a lipid droplet (LD) via autophagy in adipose tissue and the liver. We recently found that atRA induces lipophagy in adipocytes. However, it remains unclear whether atRA induces lipophagy in hepatocytes. In this study, we investigated the effects of atRA on lipophagy in Hepa1c1c7 cells and the liver of mice fed a high-fat diet (HFD). First, we confirmed that atRA induced autophagy in Hepa1c1c7 cells by Western blotting and the GFP-LC3-mCherry probe. Next, we evaluated the lipolysis in fatty Hepa1c1c7 cells treated with the knockdown of Atg5, an essential gene in autophagy induction. Atg5-knockdown partly suppressed the atRA-induced lipolysis in fatty Hepa1c1c7 cells. We also found that atRA reduced the protein, but not mRNA, expression of Rubicon, a negative regulator of autophagy, in Hepa1c1c7 cells and the liver of HFD-fed mice. Rubicon-knockdown partly inhibited the atRA-induced lipolysis in fatty Hepa1c1c7 cells. In addition, atRA reduced hepatic Rubicon expression in young mice, but the effect of atRA on it diminished in aged mice. Finally, we investigated the mechanism underlying reduced Rubicon protein expression by atRA in hepatocytes. A protein synthesis inhibitor, but not proteasome or lysosomal inhibitors, significantly blocked the reduction of Rubicon protein expression by atRA in Hepa1c1c7 cells. These results suggest that atRA may promote lipophagy in fatty hepatocytes by reducing hepatic Rubicon expression via inhibiting protein synthesis.","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100598"},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11381443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141734340","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Dietary modulation of Lp(a): more questions than answers. 膳食调节脂蛋白（a）：问题多于答案。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-07-10 DOI: 10.1016/j.jlr.2024.100592

Penny M Kris-Etherton, Terrence M Riley, Kristina S Petersen

引用次数: 0

Novel insights into the modulation of the voltage-gated potassium channel K_V1.3 activation gating by membrane ceramides. 膜神经酰胺对电压门控钾通道 KV1.3 激活门控的新见解。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-07-15 DOI: 10.1016/j.jlr.2024.100596

Bence Cs Szabo, Mate Szabo, Peter Nagy, Zoltan Varga, Gyorgy Panyi, Tamas Kovacs, Florina Zakany

{"title":"Novel insights into the modulation of the voltage-gated potassium channel KV1.3 activation gating by membrane ceramides.","authors":"Bence Cs Szabo, Mate Szabo, Peter Nagy, Zoltan Varga, Gyorgy Panyi, Tamas Kovacs, Florina Zakany","doi":"10.1016/j.jlr.2024.100596","DOIUrl":"10.1016/j.jlr.2024.100596","url":null,"abstract":"Membrane lipids extensively modulate the activation gating of voltage-gated potassium channels (KV), however, much less is known about the mechanisms of ceramide and glucosylceramide actions including which structural element is the main intramolecular target and whether there is any contribution of indirect, membrane biophysics-related mechanisms to their actions. We used two-electrode voltage-clamp fluorometry capable of recording currents and fluorescence signals to simultaneously monitor movements of the pore domain (PD) and the voltage sensor domain (VSD) of the KV1.3 ion channel after attaching an MTS-TAMRA fluorophore to a cysteine introduced into the extracellular S3-S4 loop of the VSD. We observed rightward shifts in the conductance-voltage (G-V) relationship, slower current activation kinetics, and reduced current amplitudes in response to loading the membrane with C16-ceramide (Cer) or C16-glucosylceramide (GlcCer). When analyzing VSD movements, only Cer induced a rightward shift in the fluorescence signal-voltage (F-V) relationship and slowed fluorescence activation kinetics, whereas GlcCer exerted no such effects. These results point at a distinctive mechanism of action with Cer primarily targeting the VSD, while GlcCer only the PD of KV1.3. Using environment-sensitive probes and fluorescence-based approaches, we show that Cer and GlcCer similarly increase molecular order in the inner, hydrophobic regions of bilayers, however, Cer induces a robust molecular reorganization at the membrane-water interface. We propose that this unique ordering effect in the outermost membrane layer in which the main VSD rearrangement involving an outward sliding of the top of S4 occurs can explain the VSD targeting mechanism of Cer, which is unavailable for GlcCer.","PeriodicalId":16209,"journal":{"name":"Journal of Lipid Research","volume":" ","pages":"100596"},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11367112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141633697","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction: Unmasking crucial residues in adipose triglyceride lipase for coactivation with comparative gene identification-58. 更正：通过比较基因鉴定揭示脂肪甘油三酯脂肪酶共激活的关键残基-58。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-08-10 DOI: 10.1016/j.jlr.2024.100613

Natalia Kulminskaya, Carlos Francisco Rodriguez Gamez, Peter Hofer, Ines Kathrin Cerk, Noopur Dubey, Roland Viertlmayr, Theo Sagmeister, Tea Pavkov-Keller, Rudolf Zechner, Monika Oberer

引用次数: 0

The role of ceramides in the disruption of the cutaneous permeability barrier, a common manifestation of skin disorders. 神经酰胺在皮肤渗透屏障破坏中的作用--皮肤病的一种常见表现。

IF 5 2区医学

Journal of Lipid Research Pub Date : 2024-08-01 Epub Date: 2024-07-11 DOI: 10.1016/j.jlr.2024.100593

Kenneth R Feingold, Peter M Elias

引用次数: 0