BBA Advances最新文献

{"title":"miR-765 induces angiogenesis by inhibiting dipeptidyl peptidase 4 and increasing fibroblast growth factor 2","authors":"Koji Ueno ,&nbsp;Hiroshi Kurazumi ,&nbsp;Junichi Murakami ,&nbsp;Takahiro Mizoguchi ,&nbsp;Ryo Suzuki ,&nbsp;Toshiki Tanaka ,&nbsp;Kimikazu Hamano","doi":"10.1016/j.bbadva.2026.100193","DOIUrl":"10.1016/j.bbadva.2026.100193","url":null,"abstract":"<div><div>Given that extracellular vesicles (EVs) secreted from stem cells contain angiogenic microRNAs (miRNAs), these EVs show equivalent angiogenic therapeutic effect to cell transplantation. This study aimed to identify the angiogenic miRNAs from several miRNAs involved in EVs secreted from stem cells. In human dental pulp stem cells (hDPSCs) under hypoxic culture, vascular endothelial growth factor (VEGF) involved in EVs increased. We hypothesized that angiogenic miRNAs increase in EVs that are secreted from hDPSCs under hypoxic culture compared with those under normoxic culture. In the first screening, the expression levels of miRNAs involved in EVs that were secreted from hDPSCs cultured under hypoxic and normoxic conditions were analyzed using miRNA array. In the second screening, 12 miRNAs were individually involved in EVs, and the growth of human aortic endothelial cells was assayed. In the third screening, miRNA-encapsulated EVs were injected in BALB/c mouse hindlimb ischemia model, followed by angiogenesis evaluation by blood flow analysis. Results showed that miR-765 is an angiogenic miRNA, targeting the 3′ untranslated region of dipeptidyl peptidase 4 (DPP4) and upregulating fibroblast growth factor 2 (FGF2) in vitro and in vivo. In conclusion, as an angiogenesis mechanism, miR-765 increased FGF2 expression levels by inhibiting DPP4.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100193"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147858176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural modification of 5-alkyl-4-phenyl-thiazole-based fatty acid amide hydrolase and soluble epoxide hydrolase inhibitors to alleviate orofacial inflammatory pain in the rat","authors":"Gabrielle Gorostiza ,&nbsp;Madison Mercado ,&nbsp;Lucy Pavana ,&nbsp;Daniel Carr ,&nbsp;Cassandra Yuan ,&nbsp;Amanda Tsang ,&nbsp;Karen Gomez ,&nbsp;Ian Minton ,&nbsp;Dylan Carrillo ,&nbsp;Manuel Berumen ,&nbsp;Stevan Pecic ,&nbsp;Ram Kandasamy","doi":"10.1016/j.bbadva.2026.100191","DOIUrl":"10.1016/j.bbadva.2026.100191","url":null,"abstract":"<div><div>Orofacial pain is difficult to manage. Treatments like nonsteroidal anti-inflammatory drugs (NSAIDs), and serotonin agonists provide limited relief or produce side effects. These limitations highlight the need for alternative strategies that reduce orofacial pain without adverse effects. One approach is polypharmacology, where a single compound modulates multiple targets involved in pain. Fatty acid amide hydrolase (FAAH) and soluble epoxide hydrolase (sEH) are regulators of pain that can be targeted simultaneously to enhance antinociceptive efficacy. We previously reported that the 4-phenylthiazole-based dual FAAH/sEH inhibitor <strong>SW-17</strong> does not alleviate acute orofacial pain in rats, and it showed low stability in rat liver microsomes. We introduced electronic and steric modifications to the thiazole and phenyl rings of the 4-phenylthiazole scaffold to improve the stability and better understand structure-activity relationship of this set of analogs. An 11-compound library was synthesized by varying alkyl groups at position 5 of the thiazole ring and substituents on the phenyl ring. Several analogs exhibited nanomolar potency at both enzymes. The most potent compound, <strong>4j</strong>, exhibited IC₅₀ values of 18.7 nM and 25.1 nM for human FAAH and sEH, respectively. <strong>4j</strong> was evaluated in rat liver microsomes where it exhibited relatively low metabolic stability but better than <strong>SW-17</strong>. ADMET studies indicated that <strong>4j</strong> possesses promising safety features. At 3 mg/kg, <strong>4j</strong> reversed acute orofacial inflammatory pain, whereas <strong>SW-17</strong> was ineffective. This effect was comparable to sumatriptan and did not reduce voluntary wheel running. These findings imply that optimized dual FAAH/sEH inhibitors can alleviate orofacial pain without affecting normal behavior.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100191"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147749107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inhibitors of phosphodiesterase 1 enhance paclitaxel cytotoxicity in a MDA-MB-231-derived cell line by promoting microtubule stabilization","authors":"Hsiao-Hui Kuo,&nbsp;Chien-Wei Huang,&nbsp;Tsai-Ming Lu,&nbsp;Wei-Rou Chiang,&nbsp;Ling-Huei Yih","doi":"10.1016/j.bbadva.2026.100187","DOIUrl":"10.1016/j.bbadva.2026.100187","url":null,"abstract":"<div><div>Resistance of tumor cells to chemotherapy remains a critical obstacle to effective cancer treatment. Although paclitaxel is one of the most commonly used chemotherapeutic agents for treating triple-negative breast cancer (TNBC), the mechanisms underlying paclitaxel resistance are not fully understood. We previously found that phosphodiesterase 1C (PDE1C) was substantially upregulated in a paclitaxel-resistant T50RN cell clone established from the human TNBC cell line MDA-MD-231. In this study, we aimed to explore whether and how PDE1C modulates resistance to paclitaxel in T50RN cells. Our results showed that depletion of PDE1C enhanced paclitaxel cytotoxicity, and that pharmacological inhibition of PDE1 potentiated paclitaxel-induced antiproliferative and antimitotic effects in T50RN cells. Additionally, intracellular cyclic adenosine monophosphate (cAMP) levels were lower in T50RN cells than in parental MDA-MB-231 cells. PDE1 inhibition restored the cAMP level, suggesting that cAMP-degrading activity of PDE1 is elevated in the T50RN cells. Similar to PDE1 inhibitors, the cell permeable cAMP analog 8‑bromo-cAMP or the adenylate cyclase activator forskolin increased cAMP levels and concurrently augmented paclitaxel-induced cytotoxicity and spindle abnormalities in T50RN cells. Furthermore, PDE1 inhibitors, forskolin, and an agonist of the cAMP downstream effector EPAC enhanced paclitaxel-mediated microtubule (MT) stabilization. Thus, PDE1 inhibition may act through cAMP/EPAC signaling to facilitate MT stabilization and potentiate the antiproliferative and antimitotic effects of paclitaxel in T50RN cells. Upon PDE1 inhibition, paclitaxel-treated T50RN cells exhibited signs of endoplasmic reticulum (ER) stress and apoptosis. Together, our <em>in vitro</em> findings indicate that PDE1C overexpression contributes to paclitaxel resistance.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100187"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147656322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PTC124 promotes mutation site–dependent readthrough of STK11 nonsense mutations and restores tumor suppressor function","authors":"Chen-Hsiu Hung,&nbsp;Hsiao-Hsuan Wang,&nbsp;Yi-Ting Cheng,&nbsp;Jing-Yan Chen,&nbsp;Kuan-Yu Lin,&nbsp;Sih-Tong Chen,&nbsp;Tzu-Ying Pan,&nbsp;Hung-Jui Lin,&nbsp;Chia-Chi Chen,&nbsp;Bi-He Cai","doi":"10.1016/j.bbadva.2026.100201","DOIUrl":"10.1016/j.bbadva.2026.100201","url":null,"abstract":"<div><div>Nonsense mutations in the tumor suppressor gene STK11 result in loss of tumor-suppressive function, contributing to cancer progression. PTC124 (Ataluren), a small-molecule compound that promotes ribosomal readthrough of premature stop codons, has emerged as a potential strategy to restore protein expression in such contexts. In this study, PTC124 treatment successfully restored detectable STK11 protein expression in cancer cells harboring specific nonsense mutations. Notably, the readthrough efficiency was mutation-dependent, with preferential rescue observed in N-terminal rather than C-terminal STK11 nonsense mutations. Functionally, restoration of STK11 expression led to activation of the AMPK signaling pathway and subsequent suppression of tumor cell growth. Pharmacological inhibition of AMPK attenuated these effects, further supporting that the antitumor activity of PTC124 is mediated through the STK11–AMPK signaling axis. Collectively, these findings highlight the therapeutic potential of nonsense mutation readthrough strategies and suggest that PTC124 may serve as a precision medicine approach for cancers harboring STK11 nonsense mutations.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"10 ","pages":"Article 100201"},"PeriodicalIF":4.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148776631","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic changes and roles of LYVE-1 during lipopolysaccharide-induced ALI/ARDS in mice","authors":"Shuntaro Matsunaga,&nbsp;Shinnosuke Takamori,&nbsp;Shen Lin,&nbsp;Chen Man,&nbsp;Yukie Mizuta,&nbsp;Sayoko Narahara,&nbsp;Takahito Kawano,&nbsp;Masaharu Murata,&nbsp;Tomohiko Akahoshi","doi":"10.1016/j.bbadva.2026.100202","DOIUrl":"10.1016/j.bbadva.2026.100202","url":null,"abstract":"<div><h3>Background</h3><div>Lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) has been recognized as a marker of lymphatic vessels; however, recent studies have reported that LYVE-1 is expressed in diverse cell types and functionally contributes to organ repair. Herein, we examined the expression pattern of LYVE-1 in acute respiratory distress syndrome (ARDS) model mice.</div></div><div><h3>Methods</h3><div>Acute lung injury (ALI) was induced by intratracheal administration of lipopolysaccharide (LPS) in mice. The expression and localization of LYVE-1 during the inflammatory and resolution phases were assessed by immunohistochemistry and western blot analysis. We also assessed the extent of lung injury following pharmacological inhibition of LYVE-1.</div></div><div><h3>Results</h3><div>During the inflammatory phase of lung injury, 6 h after LPS treatment, a marked decrease in LYVE-1 expression was observed, accompanied by the accumulation of hyaluronan in the tissue. During the repair process at 12 and 24 h, LYVE-1 expression transiently increased beyond baseline levels before returning to a steady state. Notably, LYVE-1-positive M2 macrophages were detected during the resolution phase. Furthermore, LYVE-1 inhibition exacerbated the severity of lung injury and resulted in poor prognosis.</div></div><div><h3>Conclusion</h3><div>LYVE-1 exhibits dynamic expression during lung inflammation and repair, not only in lung tissues but also in M2-like macrophages. Therefore, LYVE-1 may serve as a target for future pharmacological interventions in ALI.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"10 ","pages":"Article 100202"},"PeriodicalIF":4.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13560032/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148945779","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The long non-coding RNA LINC01089 facilitates prostate cancer progression","authors":"Sandra Vega Neira,&nbsp;Damu Tang","doi":"10.1016/j.bbadva.2026.100205","DOIUrl":"10.1016/j.bbadva.2026.100205","url":null,"abstract":"<div><h3>Background</h3><div>Evidence suggests LINC01809 being involved in prostate cancer (PC). We studied LINC01089 functionality, the underlying mechanisms, and translational potential in PC.</div></div><div><h3>Methods</h3><div>Multiple PC cohorts (local, TCGA, and others) were utilized. Human (DU145 and LNCaP) and murine (TRAMP-C2) PC cells were used to investigate LINC01089-derived oncogenic potential in vitro and in vivo.</div></div><div><h3>Results</h3><div>LINC01089 upregulation occurred in PC, Gleason score 9–10 tumors and metastasis. LINC01089 stratified PC recurrence. Plasma collected from patients (n = 235) prior to treatment contained elevated LINC01089, which was further increased in higher Gleason PCs and modestly correlated with PSA score. LINC01089-positively correlated genes contained a 15-gene panel (Sig15) and were dominantly enriched in RNA splicing in multiple PC datasets, with three genes (DDX17, LUC7L3, and HNRNPH1/Overlap3) conserved. Overlap3 and Sig15 effectively stratified the recurrence risk of PC and poor prognosis across 9 other cancer types, and captured the tumors' RNA splicing property, a major mechanism contributing to androgen receptor (AR) variants. Ectopic LINC01089 enhanced DU145, LNCaP, and TRAMP-C2 PC cell proliferation, colony formation, and migration, and conferred LNCaP and TRAMP-C2 cell proliferation under androgen deprivation, along with AR upregulation in the nucleus. In C57BL/6 mice, TRAMP-C2 LINC01089 allografts grew faster and expressed increased nuclear AR, Ki67, and AKT activation. TRAMP-C2 LINC01089 allografts expressed higher levels of Overlap3 and some Sig15 genes.</div></div><div><h3>Conclusion</h3><div>LINC01089 facilitates PC. Overlap3 and Sig15 are novel prognostic biomarkers reflecting cancer-associated RNA splicing. Plasma LINC01089 displays PC diagnostic potential.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"10 ","pages":"Article 100205"},"PeriodicalIF":4.5,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149211247","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adjacent domains drive the emergence of misfolded intermediates in the folding pathway of the PDZ4 from MAGI1","authors":"Valeria Pennacchietti ,&nbsp;Cosmin Marian Obreja ,&nbsp;Dimitrios Marinidis ,&nbsp;Sara Di Matteo ,&nbsp;Rodolfo Ippoliti ,&nbsp;Stefano Gianni ,&nbsp;Francesca Malagrinò","doi":"10.1016/j.bbadva.2026.100184","DOIUrl":"10.1016/j.bbadva.2026.100184","url":null,"abstract":"<div><div>Protein misfolding in multidomain assemblies emerges from a complex interplay between intra- and interdomain interactions. Here, we dissect how neighboring domains shape the folding and misfolding of the PDZ4 domain from the scaffold protein MAGI1. Exploiting the single intrinsic tryptophan in PDZ4, we monitored its behavior in the isolated domain, in the PDZ3–4 tandem, and within the five-domain PDZ2–6 supramodule by equilibrium and kinetic (un)folding experiments over a broad pH range. Equilibrium denaturation reveals that PDZ4 displays a cooperative, two-state-like transition with similar thermodynamic stability in all constructs, indicating that domain adjacency does not appreciably affect its native state. In contrast, kinetic measurements uncover pronounced deviations from two-state behavior. PDZ4 alone populates a transient intermediate, whose population and associated kinetic slowdown are markedly amplified in the tandem and even more in the supramodular context, consistent with the formation of a misfolded ensembles stabilized by non-native interdomain contacts. Acidic pH selectively enhances the kinetic trap in PDZ3–4 and PDZ2–6, but not in PDZ4 alone, pointing to a key role of electrostatics at interdomain interfaces, potentially involving specific salt bridges. Structural inspection suggests the presence of potential specific salt bridges (Asp871/Glu901 with Arg873/Lys905), although further investigation is required. Our data show that misfolding of MAGI1 PDZ4 is a context-dependent, cooperative property of adjacent domains rather than a simple by-product of folding, and illustrate how supramodular organization encodes kinetic plasticity in scaffold proteins.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100184"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147395490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AGTRAP mediates exosome-driven communication between cancer cells and macrophages via p38 MAPK pathway to promote hepatocellular carcinoma","authors":"Shanshan Liu ,&nbsp;Zhenghang Li ,&nbsp;Hongqing Liu ,&nbsp;Xinyu Chen ,&nbsp;Yilin Liu ,&nbsp;Jun Tang ,&nbsp;Yanlin Chen ,&nbsp;Dan Zeng","doi":"10.1016/j.bbadva.2026.100189","DOIUrl":"10.1016/j.bbadva.2026.100189","url":null,"abstract":"<div><h3>Background</h3><div>Angiotensin II Receptor-Associated Protein (AGTRAP) is markedly overexpressed in hepatocellular carcinoma (HCC) cases associated with poor prognosis; however, its precise functional role remains inadequately elucidated.</div></div><div><h3>Objective</h3><div>This study aimed to elucidate the functional role of AGTRAP in HCC progression and its impact on the tumor microenvironment (TME).</div></div><div><h3>Methods</h3><div>We knocked down AGTRAP expression in HCC cell lines (HepG2 and SK-hep1) using shRNA and evaluated the impact of AGTRAP knockdown on hepatocellular carcinoma cells through proliferation, invasion, and migration. Immunofluorescence staining was used to analyze the distribution of M1-type and M2-type macrophages in HCC patient tissues. The signaling pathway mechanism by which AGTRAP regulates macrophage polarization was further analyzed, focusing on the p38 MAPK pathway. The effects and mechanisms of exosomes derived from AGTRAP-knockdown HCC cells on macrophage polarization were investigated.</div></div><div><h3>Results</h3><div>Silencing AGTRAP significantly enhanced apoptosis, disrupted cell cycle progression, and diminished the invasive and migratory capacities of HCC cells.Tumors with high AGTRAP expression exhibited increased M2-type macrophages and decreased M1-type macrophages, indicating a shift in the TME towards an immunosuppressive state.Mechanistic studies revealed that AGTRAP modulates macrophage polarization by interacting with the p38 MAPK signaling pathway.Exosomes derived from AGTRAP-silenced HCC cells also influenced macrophage polarization via the p38 MAPK pathway.</div></div><div><h3>Conclusion</h3><div>AGTRAP facilitates HCC progression by mediating exosomal communication between cancer cells and macrophages via the p38 MAPK pathway, underscoring its pivotal role in shaping the immunosuppressive tumor microenvironment.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100189"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147843700","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioactive derivatives of the antimicrobial peptide esculentin-1a promote human dermal fibroblast migration and activate genes involved in early wound healing","authors":"Floriana Cappiello ,&nbsp;Eleonora Grisard ,&nbsp;Alice Traversa ,&nbsp;Danilo Ranieri ,&nbsp;Maria Luisa Mangoni","doi":"10.1016/j.bbadva.2026.100186","DOIUrl":"10.1016/j.bbadva.2026.100186","url":null,"abstract":"<div><div>Antimicrobial peptides (AMPs) are essential components of the innate immune system and have emerged as promising candidates against antibiotic-resistant infections. Beyond their antimicrobial activity, AMPs also play a crucial role in regulating tissue regeneration processes, including wound healing. Previous studies have shown that the frog skin-derived AMP, esculentin-1a(1-21) [Esc(1-21)], promotes wound healing by accelerating keratinocyte migration. Its derivative, esculentin-1a(1-21)-1c [Esc(1-21)-1c] has proven even more effective in facilitating wound closure in alveolar and bronchial epithelial cell monolayers. Given the essential role of dermal fibroblasts in skin regeneration, this study aimed to investigate the effects of Esc(1-21) and its two derivatives, Esc(1-21)-1c and [Aib⁸]-Esc(1-21) (containing the non-natural α-aminoisobutyric acid at position 8), on the activation of human primary dermal fibroblasts (hDFs) during the healing of a pseudo-wound. The results demonstrated that all three peptides significantly enhanced hDFs migration and stimulated wound closure by activating the MAPK/ERK signaling pathway, without affecting cell proliferation. Importantly, for Esc(1-21) and [Aib⁸]-Esc(1-21), this activation was clearly mediated by Epidermal Growth Factor Receptor (EGFR). Finally, the peptides upregulated the expression of early wound healing markers, such as Collagen I and Collagen III, but did not alter the expression of late-stage markers, including MMP9 and α-SMA. These findings highlight the regenerative potential of Esc(1-21) and its derivatives and suggest their relevance in therapeutic strategies for impaired wound healing.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100186"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147612145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thermodynamic signatures in ß-oxidation drive selective mobilization of fatty acids during negative energy balance in white adipose tissues","authors":"Natarajan Ganesan","doi":"10.1016/j.bbadva.2026.100181","DOIUrl":"10.1016/j.bbadva.2026.100181","url":null,"abstract":"<div><div>A theoretical model of mitochondrial β-oxidation efficiency is presented, using ATP yield per oxygen atom (P:O_β-ox) as a proxy for performance under oxygen-limited conditions. Expressed as a function of chain length and unsaturation, the model generates hyperbolic efficiency surfaces whose maxima mirrors the natural abundance of fatty acids in adipose tissues. It predicts a crossover near <em>d</em> ≈ 1.6, where efficiency becomes chain-length–independent—thus matching the dominance of monounsaturated FAs in mammals. The model aligns with empirical mobilization patterns and suggests an oxygen- and ATP-sensitive regulatory axis shaping lipid profiles in hypoxic or energy-stressed states.</div></div>","PeriodicalId":34672,"journal":{"name":"BBA Advances","volume":"9 ","pages":"Article 100181"},"PeriodicalIF":3.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146188279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}