Bioscience Reports最新文献

{"title":"Association of vitamin B1/B6/B12 supplementation with sphingosine-1-phosphate signaling and its receptors in multiple sclerosis patients: relevance to LISPR1 and APOA1-AS.","authors":"Noha A Mehana, Heba R Ghaiad, Mohammed M Nooh, Mai A Amer, Lobna Talaat El-Ghoneimy, Maheera H Safwat","doi":"10.1042/BSR20260065","DOIUrl":"https://doi.org/10.1042/BSR20260065","url":null,"abstract":"<p><p>MS is a lifelong autoimmune disorder striking the central nervous system (CNS). Despite the currently used disease-modifying therapies, patients are exposed to persistent neuropathy, pinpointing the need for supportive therapy. Neurotropic vitamins B1, B6 and B12 have been used to offer relief from immunological and neurological MS manifestations. This study aimed to provide some mechanistic insights into the relationship of B1/B6/B12 vitamin supplementation with the development of MS regarding lipid metabolism and epigenetics. In this cross-sectional observational study, blood samples were obtained from 53 MS patients, including 25 patients who had received daily vitamin B1/B6/B12 supplementation for over six months and 28 patients without supplementation. Plasma sphingosine-1-phosphate (S1P) and S1P receptor-1 (S1PR1) levels, lipid profile, and gene expression of ApoA1, sphingosine kinases 1&2 (SPHK1&2), S1PR1, as well as the lnc RNAs APOA1-AS and LISPR1 were evaluated. Gene ontology and KEGG pathway enrichment analyses were conducted. Vitamin B1/B6/B12 supplementation was associated with a more favorable lipid profile. Supplemented patients also exhibited higher ApoA1 and lower APOA1-AS expression compared with non-supplemented patients. Additionally, vitamin B1/B6/B12 supplementation was associated with lower expression levels of SPHK1, SPHK2, LISPR1, and S1PR1, and reduced circulating S1P concentrations. These findings imply significant associations between long-term vitamin B1/B6/B12 supplementation, alterations in lipid-related markers and sphingosine-associated signaling in MS patients. However, the observational design, selection bias and small sample size limit causal inference and may not fully capture the heterogeneity of MS population. Besides, supplement adherence was self-reported and not objectively verified, and circulating vitamin levels were not measured.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810571","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrative Role of Orexigenic Peptides in Neuroprotection and Neurodegenerative Disease Modulation.","authors":"Zuzana Sopko, Andrea Pačesová, Blanka Železná, Lenka Maletinska","doi":"10.1042/BSR20250362","DOIUrl":"https://doi.org/10.1042/BSR20250362","url":null,"abstract":"<p><p>The neuroprotective properties of several anorexigenic peptides, including leptin and GLP-1, are well established across models of neurodegenerative diseases. However, less is known about the role of orexigenic neuropeptides-including neuropeptide Y, agouti-related peptide, melanin-concentrating hormone, orexins, galanin, and peripherally released hormone ghrelin- that are best known for their role in energy balance and stimulation of food intake. Growing evidence highlights their broader neuroprotective properties across preclinical models of Alzheimer's disease (AD) and Parkinson's disease (PD). In AD, these peptides reduce hallmark pathologies such as amyloid burden, tau phosphorylation, oxidative stress, and neuroinflammation, while enhancing synaptogenesis, neurogenesis, and cognitive function. In PD models, ghrelin protects nigrostriatal dopaminergic neurons by restoring autophagic flux, suppressing endoplasmic reticulum stress-mediated apoptosis, and reducing microglial activation, whereas orexin A and B preserve tyrosine hydroxylase expression, promote neuronal excitability, and improve motor and cognitive outcomes. Taken together, these findings position orexigenic peptides as promising modulators of neurodegeneration and highlight their potential as potential therapeutic targets in AD and PD.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural characterization of the human CC2D1A fragment associated with non-syndromic intellectual disability (NSID).","authors":"Yi-Hung Yeh, Min-Guan Lin, Xing-Han Sun, Yo-You Shen, Pin Ling, Chwan-Deng Hsiao","doi":"10.1042/BSR20253955","DOIUrl":"https://doi.org/10.1042/BSR20253955","url":null,"abstract":"<p><p>CC2D1A is a multidomain scaffold protein implicated in transcriptional regulation and autosomal recessive non-syndromic intellectual disability (NSID), yet its molecular mechanism is still poorly understood due to a lack of structural information. Here, we present the crystal structure of the human CC2D1A₄₉₁-₈₁₀ fragment, encompassing the fourth DM14 domain, a coiled-coil region, and a C-terminal C2 domain. These elements form a compact, integrated architecture, with the C2 domain mediating symmetric dimerization through conserved electrostatic interactions. In addition, a unique antiparallel β1-β10 sheet connects the coiled-coil and C2 domains stabilizing the tertiary structure. Fluorescence polarization assays reveal micromolar DNA-binding affinity, likely mediated by the basic surface of the DM14 domain. Comparison with the Drosophila homolog Lgd highlights conserved topology with added structural features, offering insights into CC2D1A's vertebrate-specific functions and NSID-related mutations.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Conserved rod-to-spherical shape transitions in Escherichia coli through primordial experimental adaptations.","authors":"Hui Lu, Yueyue Zhang, Boying Xu, Di Tian, Yang Xia, Tetsuya Yomo, Jian Xu","doi":"10.1042/BSR20260045","DOIUrl":"https://doi.org/10.1042/BSR20260045","url":null,"abstract":"<p><p>Cell shape plays a fundamental role in bacterial physiology, yet the evolutionary stability of morphological adaptations remains poorly understood. Our previous work suggested that Escherichia coli can evolve a spherical form under primordial‑like conditions. Here, we extended experimental evolution for approximately 1000 generations in oleic acid vesicle (OAV)‑supplemented media mimicking primordial environments, followed by 500 generations in glucose. We observed a robust and stable transition from rod‑shaped to spherical morphology that persisted despite environmental reversal. This morphological shift was accompanied by mutations in cell‑shape‑related genes, and no reversion to the ancestral rod shape was observed during evolution in glucose, where mutations primarily affected metabolic and transcriptional pathways. These findings show that environmental pressures can drive heritable and evolutionarily stable morphological changes in bacteria. Our work provides insight into the genetic and environmental factors shaping bacterial cell geometry and is consistent with, though not conclusive for, the possibility that primordial cells may have been spherical.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761292","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Small-molecule inhibitor of Gαo for GNAO1 encephalopathy.","authors":"Yonika A Larasati, Alexey Koval, Vladimir L Katanaev","doi":"10.1042/BSR20250392","DOIUrl":"https://doi.org/10.1042/BSR20250392","url":null,"abstract":"<p><p>GNAO1-related neurodevelopmental disorders are caused by mutations in the GNAO1 gene encoding the major neuronal G protein, Gαo. GNAO1 encephalopathies manifest in a range of symptoms, including epilepsy, movement disorder, hypotonia, and developmental delay, affecting >400 patients worldwide to date. A growth in the number of diagnosed cases is expected due to the wider availability of whole genome sequencing.  One of the most recurrent pathogenic variants causing GNAO1 encephalopathy is an intronic mutation c.724-8G>A, which results in an in-frame insertion of two amino acid residues Pro-Gln after Thr241: Gαo[T241_N242insPQ]. We previously performed in-depth profiling of Gαo[insPQ] using structural, biochemical, and cellular studies. Compared to the wild-type protein, Gαo[insPQ] exhibits faster GTP binding and decreased hydrolysis. Importantly, Gαo[insPQ] is deficient in interacting with regulators of G protein signaling (RGS), GTPase-activating proteins that deactivate Gαo. These defects render Gαo[insPQ] as a constitutively active mutant loaded with GTP in the G protein signaling. Patients harboring Gαo[insPQ] variant are in urgent need of novel therapy as they are refractory to available medications. In this study, we performed a high-throughput screening to find molecules that might suppress the constitutive GTP loading by Gαo[insPQ]. We used a high-diversity chemical library of 54,080 compounds, identifying a novel compound, N-[5-(2-methylpropyl)-1,3,4-thiadiazol-2-yl]-1H-1,2,3-benzotriazole-5-carboxamide, that decreases the GTP binding rate of Gαo, likely acting as a competitive inhibitor with higher selectivity to the pathogenic protein. This small-molecule inhibitor of Gαo opens new opportunities to drug discovery towards Gαo-dependent pathologies.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aerobic  Exercise Is Associated with Divergent Regulation of Macrophage Migration Inhibitory Factor and Enhanced Remyelination in Experimental Autoimmune Neuritis.","authors":"Yantong Liu, Xiaohan Shi, Ying Wang, Yunhao Deng, Haoyue Chen, Hao Zhang, Yuwen Hao, Ling Zheng, Xiaoyu Wang, Zuncheng Zheng, Kai Wang, Xiaojing Yuan","doi":"10.1042/BSR20260227","DOIUrl":"https://doi.org/10.1042/BSR20260227","url":null,"abstract":"<p><p>This study investigated the association between aerobic exercise preconditioning and macrophage migration inhibitory factor (MIF) expression, as well as myelination in sciatic nerve in experimental autoimmune neuritis (EAN) rats. Female Lewis rats underwent 4-week swimming protocols including High-intensity daily (HI-Daily), Moderate-intensity daily (MOD-Daily), and Moderate-intensity alternate-day (MOD-AltDay) regimens prior to EAN induction, with control groups of EAN without exercise and Sham operation. Assessment of disease severity, nerve conduction velocity, and sciatic nerve pathology revealed that the moderate-intensity alternate-day exercise regimen significantly delayed disease onset, lowered peak clinical scores, and improved neurological function. Molecular analyses demonstrated that this protective effect was mediated through divergent regulation of MIF: systemic MIF was substantially suppressed (27205.94 ± 4291.76 pg/mL vs EAN 71075.61 ± 10166.41 pg/mL; p<0.001) with concomitant reduction in macrophage infiltration, while local MIF expression within the sciatic nerve was significantly elevated (p<0.01), correlating with enhanced remyelination as evidenced by increased myelin sheath area (LFB: 67.42 ± 3.26% vs EAN 40.64 ± 9.63%, p<0.01) and elevated myelin basic protein expression (0.92 ± 0.14 AU vs EAN 0.59 ± 0.02 AU, p<0.05). Crucially, both high-intensity daily and moderate-intensity daily exercise protocols failed to confer comparable benefits. These findings indicate that the protective effect of MOD-AltDay exercise preconditioning on EAN is associated with tissue-specific regulation of MIF, and this change correlates with reduced systemic inflammation and enhanced local remyelination. Pharmacological/genetic studies are needed to confirm mechanisms and evaluate this exercise regimen as a non-pharmacological intervention for autoimmune neuropathy.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761298","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Engineering extracellular vesicles for targeted therapeutic delivery in the heart.","authors":"Iqra Anwar, Xinghua Wang, Saverio Parlongo, Sonalí Harris, Richard E Pratt, Victor J Dzau, Conrad P Hodgkinson","doi":"10.1042/BSR20254075","DOIUrl":"10.1042/BSR20254075","url":null,"abstract":"<p><p>Heart failure is a leading cause of morbidity and mortality, highlighting the need for improved therapeutic strategies. Critical to the success of therapies is efficient and targeted delivery systems. Extracellular vesicle-based delivery systems have emerged as promising candidates due to their biocompatibility and low immunogenicity. While extracellular vesicles from a wide variety of cells have been used, they have demonstrated divergent effects on the heart. The present review first summarizes the current sources of extracellular vesicles employed in heart failure therapy and their contrasting outcomes. The review then examines the view that these contrasting outcomes arise from limited cell specificity, inefficient delivery, and suboptimal cargo loading. Finally, the review discusses how these problems are being dealt with by recent advances, including genetic modification, chemical functionalization, and enhanced loading strategies. Together, these approaches highlight the potential of extracellular vesicle-based systems as precision therapeutics in cardiovascular medicine.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":"46 4","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13136563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761264","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Observation of aldicarb hydrolysis by a cocaine hydrolase.","authors":"Johnathan E LeSaint, Daniel J Peter, Huimei Wei, Shawn Park, Chang-Guo Zhan, Fang Zheng","doi":"10.1042/BSR20254091","DOIUrl":"10.1042/BSR20254091","url":null,"abstract":"<p><p>Aldicarb is a carbamate pesticide used for pest control in agriculture. As a fast-acting acetylcholinesterase inhibitor, aldicarb interferes with the nervous system by preventing the breakdown of acetylcholine. Aldicarb could be used as a chemical-warfare agent to cause mass casualty incidents. There is no specific FDA-approved medication for aldicarb detoxification. Our previous study revealed that an Fc-fused butyrylcholinesterase (BChE) mutant, known as CocH3-Fc(M3), can be inhibited rapidly by aldicarb and that the aldicarb-inhibited enzyme CocH3-Fc(M3) can be reactivated spontaneously, suggesting that CocH3-Fc(M3) may hydrolyze aldicarb. However, the suggested CocH3-Fc(M3)-catalyzed hydrolysis of aldicarb was not confirmed experimentally in the previous study. In the present study, by developing an LC-MS/MS method to detect and quantify aldicarb and aldicarb oxime concentrations, we were able to directly observe the CocH3-Fc(M3)-catalyzed aldicarb hydrolysis for the first time, confirming that CocH3-Fc(M3) indeed has the desirable catalytic activity for aldicarb hydrolysis and may be considered as the first aldicarb hydrolase identified so far. Further, we carried out Michaelis-Menten kinetic analysis on the CocH3-Fc(M3)-catalyzed aldicarb hydrolysis and determined the catalytic parameters (kcat = 0.060 min-1, KM = 2.5 μM, and kcat/KM = 2.4 × 104 min-1 M-1) at 37°C. The obtained kinetic parameters at 37°C will be valuable for further in vivo studies and translational research using CocH3-Fc(M3) and for designing more potent enzymes to hydrolyze aldicarb in the future. Additionally, the LC-MS/MS method developed in this study may serve as a valuable tool to accurately detect aldicarb and its reaction products in future food and environmental safety control efforts and aldicarb-related toxicology studies.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13136561/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Renal function dynamics in COVID-19: exploring biomarker interactions with D-dimer and C-reactive proteins.","authors":"Ishita Saha, Anirban Sinha, Anup Kumar Sadhu, Rabindra Nath Das, Satadru Ghosh, Priyajit Banerjee, Oly Banerjee, Shampa Sarkar Biswas, Sandip Mukherjee, Palash Kumar Pal","doi":"10.1042/BSR20254002","DOIUrl":"10.1042/BSR20254002","url":null,"abstract":"<p><p>COVID-19, caused by the SARS-CoV-2 virus, is mainly recognized for its respiratory manifestations. However, growing evidence regarding the widespread expression of ACE2 and TMPRSS2 receptors on diverse extrapulmonary sites, particularly in renal tubular epithelial cells, suggests susceptibility of other organ systems, including the kidneys, to such conditions as acute kidney injury (AKI). In the present retrospective study, we explored the interrelationship between disease severity and renal function abnormalities by analyzing key biochemical parameters: blood urea nitrogen (BUN), serum creatinine (Cr), the BUN/Cr ratio, and estimated glomerular filtration rate (eGFR). Using descriptive statistics and joint generalized linear models, we examined both the mean and variance components of these markers alongside inflammatory indicators such as C-reactive protein (CRP) and D-dimer. Our findings revealed a significant positive correlation between serum urea levels and both CRP and D-dimer concentrations, suggesting that elevated urea may reflect heightened inflammatory activity. Additionally, eGFR showed a positive association with CRP, indicating potential renal involvement in systemic inflammation. Our in silico studies supported such observations, as genes responsible for CRP and D-dimer elevation were found to be common in AKI-associated pathways, particularly IL-6/JAK-STAT, NF-κB, HIF-1, and complement pathways, ultimately causing renal microthrombosis, tubular necrosis, and fibrotic remodeling. Notably, serum Cr revealed no significant association with CRP or D-dimer, possibly due to its lower sensitivity in early renal dysfunction. Although the study is limited by a relatively small sample size and lacks longitudinal data, it underscores the importance of monitoring renal function parameters in COVID-19 patients as potential markers of disease progression.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13136562/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147637860","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox status of apolipoprotein E in cerebrospinal fluid: A mechanistically informative biomarker for central nervous system disorders.","authors":"Yui Uematsu, Wakana Iinuma, Riho Shimizu, Hiroto Matsuura, Tsuneaki Yoshinaga, Masahide Yazaki, Kazuyoshi Yamauchi","doi":"10.1042/BSR20250388","DOIUrl":"https://doi.org/10.1042/BSR20250388","url":null,"abstract":"<p><p>Apolipoprotein (apo) E is the major cholesterol carrier in the central nervous system (CNS); however, the clinical relevance of its cysteine-thiol redox status in cerebrospinal fluid (CSF) remains unclear. We investigated whether CSF apoE redox indices (redox-IDX-apoE) reflect cholesterol transport efficiency and disease-specific pathologies. We quantified reduced (red), reversibly oxidized (roxi), and irreversibly oxidized (oxi) apoE in CSF and serum using a maleimide-based band-shift assay. We analyzed relationships between redox-IDX-apoE, CSF cholesterol (TC) level, and the TC/apoE ratio (inverse transport efficiency) in patients with apoE3/E3 and identified transport determinants using isometric log-ratio (ILR) regression. Significant but only moderate correlations between CSF and serum indices suggested distinct redox behavior in the two compartments. ApoE3/E4 carriers exhibited higher oxi-apoE, reflecting reduced buffering capacity. In apoE3/E3 CSF, aging increased roxi/total and decreased red/roxi, suggesting a shift toward oxidized forms. CSF TC level positively correlated with roxi-related indices. Conversely, the TC/apoE ratio negatively correlated with red/roxi, indicating that red-apoE supports higher efficiency. ILR analysis confirmed that maintaining the reduced monomeric state, rather than the reversibly oxidized form, was independently associated with improved transport efficiency. Diagnostic groups exhibited distinct signatures: neurodegenerative disorders showed elevated irreversible oxidation, whereas neuroimmunological and infectious conditions exhibited profiles suggestive of reversible and acute oxidation, respectively. The CSF apoE redox status links local redox balance to cholesterol handling and reflects CNS pathophysiology. Maintaining reduced cysteine-thiol appears important for functional capacity, whereas a shift toward oxidation reflects a trade-off between buffering ability and transport efficiency. These indices may serve as potential biomarkers.</p>","PeriodicalId":8926,"journal":{"name":"Bioscience Reports","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}