Biochimica et biophysica acta. Molecular cell research最新文献

The dual role of heat shock protein 60 in Cardiac diseases: From mitochondrial chaperone to extracellular immunomodulator - A review and future perspectives. 热休克蛋白60在心脏疾病中的双重作用：从线粒体伴侣到细胞外免疫调节剂——综述和未来展望

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-05-02 DOI: 10.1016/j.bbamcr.2026.120154

Vahid Saqagandomabadi, Adelaide Carista, Stefano Burgio, Francesco Cappello, Valentina Di Felice

{"title":"The dual role of heat shock protein 60 in Cardiac diseases: From mitochondrial chaperone to extracellular immunomodulator - A review and future perspectives.","authors":"Vahid Saqagandomabadi, Adelaide Carista, Stefano Burgio, Francesco Cappello, Valentina Di Felice","doi":"10.1016/j.bbamcr.2026.120154","DOIUrl":"10.1016/j.bbamcr.2026.120154","url":null,"abstract":"<p><p>The abundance of mitochondria in cardiac cells is vital, as they are extremely important for adenosine triphosphate (ATP) synthesis, maintaining redox balance, regulating calcium homeostasis, and facilitating lipid synthesis. One of the most abundant proteins in the mitochondria is the heat shock protein 60 (Hsp60), a chaperone that plays a crucial role in the translocation and folding of mitochondrial proteins. As a stress protein, Hsp60 increases when the heart muscle is under pressure, such as during a heart attack or heart failure. Recently, our research group has demonstrated that Hsp60 can be released under stress conditions in small and large vesicles or freely in the cell culture medium. In this review, we have analysed the published literature to determine whether Hsp60 may function as a damage-associated molecular pattern (DAMP) protein capable of interacting with Toll-like receptors (TLRs) to modulate immune responses, and we hypothesised that Hsp60 released in small extracellular vesicles may act as an immunomodulator.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"120154"},"PeriodicalIF":3.7,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147832871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to "Thermotolerance induced at a mild temperature of 40 °C alleviates heat shock-induced ER stress and apoptosis in HeLa cells" [Biochim. Biophys. Acta - Mol. Cell Res. 1853 (2015) 52-62/PMID: 25260982]. “在40°C的温和温度下诱导的耐热性减轻热休克诱导的内质网应激和HeLa细胞凋亡”的勘误[biochem]。Biophys。分子细胞学报，1853 (2015)52-62/PMID: 25260982。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-30 DOI: 10.1016/j.bbamcr.2026.120150

Ahmed Bettaieb, Diana A Averill-Bates

引用次数: 0

LMCD1 aggravates cardiac fibrosis after myocardial infarction via activating STAT5A. LMCD1通过激活STAT5A加重心肌梗死后心肌纤维化。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-29 DOI: 10.1016/j.bbamcr.2026.120153

Haofei Kang, Jing Liu, Junjie Wang, Yunrui Zhang

{"title":"LMCD1 aggravates cardiac fibrosis after myocardial infarction via activating STAT5A.","authors":"Haofei Kang, Jing Liu, Junjie Wang, Yunrui Zhang","doi":"10.1016/j.bbamcr.2026.120153","DOIUrl":"https://doi.org/10.1016/j.bbamcr.2026.120153","url":null,"abstract":"<p><p>Cardiac fibrosis, a maladaptive remodeling process following myocardial infarction (MI), is a key driver of heart failure, the precise molecular regulators governing cardiac fibroblast activation remain incompletely understood. LIM and cysteine-rich domains 1 (LMCD1) has been shown to promote renal and lung fibrosis, but its role in cardiac fibrosis is unknown. We hypothesized that LMCD1 promoted cardiac fibrosis post-MI. Re-analysis of publicly available single-cell RNA sequencing datasets revealed a significant upregulation of LMCD1 in cardiac fibroblasts after MI. LMCD1 was upregulated in mouse hearts subjected to left anterior descending (LAD) artery ligation and in primary cardiac fibroblasts stimulated with TGF-β1. Silencing of LMCD1 improved cardiac function (increased ejection fraction and fractional shortening) and reduced fibrotic area, concomitant with decreased fibrosis-related proteins (fibronectin, COL1A1, and α-SMA). In TGF-β1-induced primary cardiac fibroblasts, LMCD1 knockdown inhibited cell proliferation and fibrosis-related proteins expression, while its overexpression showed the opposite trend. Mechanistically, pathway enrichment analysis linked LMCD1 to the IL2-STAT5 signaling. LMCD1 silencing reduced the phosphorylation and total protein levels of STAT5A in infarcted mouse heart tissues. Co-immunoprecipitation assays confirmed a direct interaction between LMCD1 and STAT5A. Furthermore, STAT5A overexpression reversed the inhibitory effect of LMCD1 knockdown on TGF-β1-induced fibrosis in primary cardiac fibroblasts. In conclusion, our study identifies LMCD1 as a novel driver of post-MI fibrosis, which functions by activating STAT5A in cardiac fibroblasts, offering a potential new target for anti-fibrotic therapy.</p>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":" ","pages":"120153"},"PeriodicalIF":3.7,"publicationDate":"2026-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147810144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to "Involvement of mitochondrial and death receptor pathways in tributyltin-induced apoptosis in rat hepatocytes" [Biochim. Biophys. Acta 1693 (2004) 15-27 (15276321)]. “线粒体和死亡受体通路在三丁基锡诱导的大鼠肝细胞凋亡中的参与”[生物化学]的更正。Biophys。Acta 1693(2004) 15-27(15276321)]。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-24 DOI: 10.1016/j.bbamcr.2026.120149

M Jurkiewicz, D A Averill-Bates, M Marion, F Denizeau

引用次数: 0

ADAM proteases in cytokine biology: Modulators of immune signaling, inflammation and cancer 细胞因子生物学中的ADAM蛋白酶：免疫信号、炎症和癌症的调节剂。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-01 Epub Date: 2026-03-22 DOI: 10.1016/j.bbamcr.2026.120137

Heba Khattab , Jelena Solujic , Mohamed I. Saad

{"title":"ADAM proteases in cytokine biology: Modulators of immune signaling, inflammation and cancer","authors":"Heba Khattab , Jelena Solujic , Mohamed I. Saad","doi":"10.1016/j.bbamcr.2026.120137","DOIUrl":"10.1016/j.bbamcr.2026.120137","url":null,"abstract":"<div><div>Ectodomain shedding, a post-translational process mediated primarily by A Disintegrin And Metalloprotease (ADAM) family members, represents a fundamental mechanism regulating intercellular communications. By cleaving the extracellular domains of membrane-anchored cytokines, receptors, growth factors, and adhesion molecules, ADAM proteases dynamically shape cytokine signaling networks that underpin immune regulation, inflammation, and tissue homeostasis. Among these enzymes, ADAM10 and ADAM17 are key effectors whose tightly controlled activity ensures the fine-tuning of pro- and anti-inflammatory pathways. Dysregulated ADAM function perturbs cytokine gradients and receptor availability, contributing to the pathogenesis of cancer, autoimmune disorders, and chronic inflammatory diseases. In this review, we provide updated perspectives on the mechanisms governing ADAM activation and substrate selectivity, including prodomain processing, trafficking, interaction with protein partners, and modulation by inflammatory stimuli. We further highlight species-specific differences and genetic polymorphisms that influence ADAM expression and catalytic efficiency, emphasizing their translational relevance in precision medicine. Collectively, delineating the ADAM/cytokine signaling axis offers crucial insights into immune homeostasis and unveils novel opportunities for therapeutic intervention in cancer and immune-mediated diseases.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 4","pages":"Article 120137"},"PeriodicalIF":3.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147503045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Pathogenic implication of the CD53 tetraspanin in immune and cancer cells CD53蛋白在免疫细胞和癌细胞中的致病意义。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-01 Epub Date: 2026-03-30 DOI: 10.1016/j.bbamcr.2026.120142

Pedro A. Lazo

{"title":"Pathogenic implication of the CD53 tetraspanin in immune and cancer cells","authors":"Pedro A. Lazo","doi":"10.1016/j.bbamcr.2026.120142","DOIUrl":"10.1016/j.bbamcr.2026.120142","url":null,"abstract":"<div><div>Tetraspanin proteins are a specific family of membrane proteins with four transmembrane domains forming a core that assembles different types of complexes by their interactions among themselves, and with other membrane, extracellular and intracellular proteins. These tetraspanin complexes modulate multiple signaling pathways and generate exosomes. Tetraspanin proteins have a heterogeneous distribution, some are expressed in many different cell types, while others are highly restricted to specific cell types. Among the latter is CD53 (TSPAN25), a tetraspanin protein that is mainly expressed in nucleated hematopoietic cells, although it has also been detected in some carcinomas. CD53 forms oligomeric complexes with other members of this protein family in cell membranes, which can assemble and release exosomes and intracellular vesicles. CD53 on the plasma membrane modulates cell adhesion, migration, cell proliferation and survival. CD53 has no known specific ligand, but its ligation with specific antibodies modulates different intracellular signals, among which is protecting cells from apoptosis that is mediated by phosphorylation and activation of Akt, increased Bcl-xL level, decreased Bax level, and reducing caspase activation. CD53 ligation also induces calcium mobilization, activation of PKC and DREAM complex, and expression of the inducible nitric oxide synthase gene resulting in increased nitric oxide production. The different biological roles of CD53 are implicated in the regulation of specific functions associated with both immune responses and tumor biology. However, the heterogeneity of the cell types and of the pathways in which CD53 participates need to be studied in combination with other tetraspanins in order to detect their cooperation and contribution in specific cell types, normal or tumoral.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 4","pages":"Article 120142"},"PeriodicalIF":3.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147589497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Signal peptide-directed proteins generated in the endoplasmic reticulum are secreted or degraded via the autophagic pathway 内质网中产生的信号肽导向蛋白通过自噬途径分泌或降解。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-01 Epub Date: 2026-03-27 DOI: 10.1016/j.bbamcr.2026.120140

Taek-Yeong Kim, Ye-Jin Cho, Kwon-Yul Ryu

{"title":"Signal peptide-directed proteins generated in the endoplasmic reticulum are secreted or degraded via the autophagic pathway","authors":"Taek-Yeong Kim, Ye-Jin Cho, Kwon-Yul Ryu","doi":"10.1016/j.bbamcr.2026.120140","DOIUrl":"10.1016/j.bbamcr.2026.120140","url":null,"abstract":"<div><div>Signal peptides (SPs) are short N-terminal sequences that direct proteins to the endoplasmic reticulum (ER). After cleavage of the SP, these proteins are mostly trafficked to the Golgi apparatus for secretion. Lipocalin-2 (LCN2), a neurotoxic secretory protein, was recently identified as a target of autophagy. The presence of an SP is a prerequisite for secretion and autophagic degradation. Based on these observations, we investigated whether the SP of LCN2 is sufficient to enable proteins to be secreted or degraded via autophagy. We fused the SP of LCN2 to a non-secretory green fluorescent protein (GFP) and found that this ER-generated GFP was either secreted or degraded via autophagy. These results indicate that the LCN2-derived SP alone is sufficient to direct proteins to the ER and subsequent secretion or autophagic degradation. This dual regulation was abolished when the SP was deleted from LCN2. Notably, the effect was preserved even when the LCN2 SP was replaced with the SP from brain-derived neurotrophic factor, another secretory protein. These results suggest that SPs with different sequences can similarly direct proteins to the ER and subsequent secretion or autophagic degradation. Furthermore, we found that even when LCN2 reached the Golgi apparatus for secretion, it could also be degraded via autophagy. Thus, we propose that SP-directed and ER-generated secretory proteins can undergo autophagic degradation during ER-Golgi transport, including at the ER, the ER-Golgi intermediate compartment, or the Golgi apparatus. Taken together, degradation of secretory proteins via autophagy suggests implications for the potential control of secretory protein homeostasis.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 4","pages":"Article 120140"},"PeriodicalIF":3.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147572053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Interaction of estrogen and interleukin 6 in the progression of lymphangioleiomyomatosis 雌激素和白细胞介素6在淋巴管平滑肌瘤病进展中的相互作用

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-04-01 Epub Date: 2026-03-31 DOI: 10.1016/j.bbamcr.2026.120143

Lulu Yang , Liting Huang , Siying Ren

{"title":"Interaction of estrogen and interleukin 6 in the progression of lymphangioleiomyomatosis","authors":"Lulu Yang , Liting Huang , Siying Ren","doi":"10.1016/j.bbamcr.2026.120143","DOIUrl":"10.1016/j.bbamcr.2026.120143","url":null,"abstract":"<div><div>Lymphangioleiomyomatosis (LAM) is an estrogen-dependent disease that promotes tumor cell growth through estrogen receptor α (ERα). Interleukin 6 (IL-6) is an important estrogen (E2) target gene; however, its role in disease progression remains unclear. In the present study, we investigated the biological functions and underlying mechanisms of action of IL-6 in E2-stimulated tuberous sclerosis complex 2 (TSC2)–deficient cells. The IL-6 levels in the lung tissue and serum of the patients were detected using immunohistochemistry and enzyme-linked immunosorbent assay (ELISA). The effects of E2 and recombinant IL-6 on ERα and IL-6 signaling and the malignant behaviors of TSC2-deficient cells were examined using western blotting, immunofluorescence, Cell Counting Kit-8 (CCK-8), colony formation, transwell, and wound healing assays. The IL-6 expression was higher in LAM lung tissues than in controls, was significantly elevated in the serum of patients with LAM, and was negatively correlated with lung function. After E2 and recombinant human IL-6 (rhIL-6) intervention in TSC2-deficient cells, the expression of IL-6 and ERα was upregulated in a time-dependent manner. Fulvestrant treatment had no significant inhibitory effect on IL-6 protein expression, whereas Stattic intervention inhibited ERα expression. The combined use of fulvestrant and Stattic significantly suppressed the proliferation and migration of TSC2-deficient cells, indicating that the IL-6/signal transducer and activator of transcription 3 (STAT3) pathway plays an important role in E2-promoted LAM progression and may serve as a potential therapeutic target for LAM.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 4","pages":"Article 120143"},"PeriodicalIF":3.7,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147600604","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Corrigendum to "Frequent EPHA2 receptor mutations in cholangiocarcinoma disrupt receptor forward signaling supporting a tumor suppressor role" [BBA Mol. Cell Res. 1873 (2026) 120081]. “胆管癌中频繁的EPHA2受体突变破坏支持肿瘤抑制作用的受体前向信号传导”的更正[BBA Mol细胞杂志，1873(2026)120081]。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-03-20 DOI: 10.1016/j.bbamcr.2026.120139

Evodie Koutouan, Alejandro Lillo, Ayano Kabashima, Jack W Sample, Danielle Carlson, Rondell Graham, Rory L Smoot, Elena B Pasquale

引用次数: 0

ADAR1 upregulates the translation of cytochrome c via the inhibition of translocation into stress granules, facilitating apoptosis by an anticancer agent ADAR1通过抑制细胞色素c转运到应激颗粒中来上调细胞色素c的翻译，促进抗癌药物的凋亡。

IF 3.7 2区生物学

Biochimica et biophysica acta. Molecular cell research Pub Date : 2026-03-01 Epub Date: 2026-01-06 DOI: 10.1016/j.bbamcr.2025.120104

Motoki Isono , Tomoka Yamakawa , Kyoka Nagaoka , Masataka Nakano , Tatsuki Fukami , Miki Nakajima

{"title":"ADAR1 upregulates the translation of cytochrome c via the inhibition of translocation into stress granules, facilitating apoptosis by an anticancer agent","authors":"Motoki Isono , Tomoka Yamakawa , Kyoka Nagaoka , Masataka Nakano , Tatsuki Fukami , Miki Nakajima","doi":"10.1016/j.bbamcr.2025.120104","DOIUrl":"10.1016/j.bbamcr.2025.120104","url":null,"abstract":"<div><div>Adenosine-to-inosine (A-to-I) RNA editing catalyzed by adenosine deaminase acting on RNA (ADAR) 1 is the most abundant RNA modification in humans. We noticed that there are multiple A-to-I RNA editing sites in the 3′-UTR of cytochrome <em>c</em> (CYCS), a mitochondrial protein involved in the initiation of apoptosis. We aimed to clarify the impact of ADAR1 on the regulation of CYCS expression, its mechanism, and its biological and pharmacological significance. In human hepatocellular carcinoma-derived HepG2 or Huh-7 cells, siRNA-mediated knockdown of ADAR1 (siADAR1) reduced CYCS protein levels without affecting mRNA levels, suggesting that ADAR1 facilitates CYCS translation. Sanger sequence analysis showed that multiple adenosines in the 3′-UTR of CYCS are highly edited by ADAR1. The CYCS protein level in HepG2 <sup><em>CYCS 3′-UTR-deleted</em></sup> cells in which the 3′-UTR of CYCS was deleted by the CRISPR/Cas9 system was not decreased by siADAR1, indicating that the 3′-UTR is required for ADAR1-dependent translational regulation. The pulldown assay revealed that siADAR1 increases the binding of CYCS mRNA to RNA-binding proteins with disordered regions, suggesting that stress granules, a membrane-less organelle formed by such proteins with intrinsically disordered regions, might trap CYCS mRNA and suppress its translation. Treatment with ISRIB, an inhibitor of stress granule formation, attenuated the siADAR1-mediated decrease in CYCS protein levels. Interestingly, sorafenib-induced apoptosis in HepG2 cells was repressed by siADAR1, but this repression was not observed in HepG2 <sup><em>CYCS 3′-UTR-deleted</em></sup> cells. Collectively, this study clarified that ADAR1 upregulates CYCS translation by inhibiting stress granule formation and thereby can facilitate anticancer agent-induced apoptosis.</div></div>","PeriodicalId":8754,"journal":{"name":"Biochimica et biophysica acta. Molecular cell research","volume":"1873 3","pages":"Article 120104"},"PeriodicalIF":3.7,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145931913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0