Cell calcium最新文献_第2页

In memoriam: Irene Schulz 1941 - 2026. 纪念：艾琳·舒尔茨1941 - 2026。

IF 4.9 2区生物学

Cell calcium Pub Date : 2026-07-01 Epub Date: 2026-04-22 DOI: 10.1016/j.ceca.2026.103136

Ole H Petersen

{"title":"In memoriam: Irene Schulz 1941 - 2026.","authors":"Ole H Petersen","doi":"10.1016/j.ceca.2026.103136","DOIUrl":"https://doi.org/10.1016/j.ceca.2026.103136","url":null,"abstract":"<p><p>Irene Schulz passed away on Sunday 29th March 2026. She made fundamental contributions to the field of Calcium Signaling and, in collaboration with the late Sir Michael Berridge, showed directly that inositol-1,4,5 trisphosphate (IP<sub>3</sub>) released Ca<sup>2+</sup> from a non-mitochondrial intracellular store that she later identified as the endoplasmic reticulum (ER). The discovery of IP<sub>3</sub> as a Ca<sup>2+</sup> releasing messenger was a momentous event in the field of signal transduction mechanisms and was foundational for the field of Ca<sup>2+</sup> Signaling. Irene was born in Berlin on 25th January 1941 and graduated from the Marie-Curie High School in Berlin in February 1960. She undertook her medical studies at the Free University of Berlin and graduated in Medicine in 1966. She then went to the US, as a Postdoctoral Fellow at the National Institutes of Health (NIH) in Bethesda. In 1967, she returned to Europe to become Group Leader at the Max-Planck-Institute for Biophysics in Frankfurt, under the directorship of Karl Ullrich. From 1976 - 1991 she was also an Associate Professor of Physiology at the JW Goethe University in Frankfurt. In 1991, Irene became a full Professor and Director of the 2nd Physiological Institute at the University of the Saarland, Homburg/Saar and was in charge of that Institute until her retirement in 2006.</p>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"136 ","pages":"103136"},"PeriodicalIF":4.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148599365","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

Single-cell analysis of sterol-induced Ca2＋ signaling in human astrocytes by dynamic mode decomposition 通过动态模式分解对人星形胶质细胞中固醇诱导的Ca2+信号的单细胞分析。

IF 4.9 2区生物学

Cell calcium Pub Date : 2026-07-01 Epub Date: 2026-07-09 DOI: 10.1016/j.ceca.2026.103167

Miklas P.W. Larsen, Line Lauritsen, Amanda T. Pauli, Rasmus Jensen, Ralf Zimmermann, Max Lehmann, Pablo Wessig, Daniel Wüstner

{"title":"Single-cell analysis of sterol-induced Ca2＋ signaling in human astrocytes by dynamic mode decomposition","authors":"Miklas P.W. Larsen, Line Lauritsen, Amanda T. Pauli, Rasmus Jensen, Ralf Zimmermann, Max Lehmann, Pablo Wessig, Daniel Wüstner","doi":"10.1016/j.ceca.2026.103167","DOIUrl":"10.1016/j.ceca.2026.103167","url":null,"abstract":"<div><div>Ca<sup>2＋</sup> signaling in astrocytes is a central mechanism of intercellular communication in the brain and plays a key role in regulating neuronal excitability, synaptic plasticity, and energy metabolism. Disruption of astrocytic Ca<sup>2＋</sup> dynamics is a characteristic of neurodegenerative diseases, as are deviations in cholesterol trafficking and metabolism, which are essential for maintaining membrane structure and function. Although recent studies have begun to explore links between Ca<sup>2＋</sup> signaling and sterol homeostasis in astrocytes, unbiased analytical workflows and mechanistic insight into how cholesterol and related sterols regulate astrocytic Ca<sup>2＋</sup> dynamics remain limited.</div><div>Here, we apply dynamic mode decomposition to dissect and classify Ca<sup>2＋</sup> signals obtained from time-lapse imaging of human astrocytes. Using both synthetic and experimental datasets, we show that delay-embedded dynamic mode decomposition combined with clustering separates heterogeneous Ca<sup>2＋</sup> activity into distinct dynamical states. This analysis reveals that increasing cholesterol levels shift astrocytes toward more active oscillatory states, whereas acute cholesterol depletion suppresses Ca<sup>2＋</sup> activity. In addition, pretreatment with the oxysterols 24-, 25-, and 27-hydroxycholesterol impaired cholesterol-induced Ca<sup>2＋</sup> oscillations.</div><div>Together, this work presents a general computational framework for decomposing and analyzing complex spatiotemporal Ca<sup>2＋</sup> signals, with broad applicability to quantitative imaging in cell biology.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"136 ","pages":"Article 103167"},"PeriodicalIF":4.9,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148454758","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","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 Role of CaV3.2 T-type calcium channels in normal hearing and acquired hearing loss CaV3.2 t型钙通道在正常听力和获得性听力损失中的作用

IF 4 2区生物学

Cell calcium Pub Date : 2026-05-01 Epub Date: 2026-04-20 DOI: 10.1016/j.ceca.2026.103138

Zain Pardawala , Dora Persic , Kriti Rajda , Teodora Gheorghe , Marco Demaria , Sonja J. Pyott

{"title":"The Role of CaV3.2 T-type calcium channels in normal hearing and acquired hearing loss","authors":"Zain Pardawala , Dora Persic , Kriti Rajda , Teodora Gheorghe , Marco Demaria , Sonja J. Pyott","doi":"10.1016/j.ceca.2026.103138","DOIUrl":"10.1016/j.ceca.2026.103138","url":null,"abstract":"<div><div>Calcium ion (Ca²⁺) dysregulation contributes to both noise-induced (NIHL) and age-related hearing loss (ARHL). Voltage-gated Ca²⁺ channels (VGCCs) regulate Ca²⁺ influx and are, therefore, candidate therapeutic targets for acquired hearing loss. The T-type channel Ca<sub>V</sub>3.2 (CACNA1H) has been proposed to influence cochlear function and vulnerability. Here, we characterized the distribution and age-dependent expression of <em>Cacna1h</em> in the mouse cochlea, and tested whether Ca<sub>V</sub>3.2 modulation could mitigate NIHL or ARHL using genetic deletion and/or pharmacological blockade. Transcriptomic analyses of isolated cochlear sensorineural and metabolic substructures showed that <em>Cacna1h</em> expression remains stable from 6 weeks to 2 years of age. Auditory brainstem responses together with immunofluorescence and quantitative image analyses revealed elevated wave I thresholds and reduced amplitudes in 6-week-old Ca<sub>V</sub>3.2 knockout (KO) compared to wildtype (WT) and heterozygous (HET) mice, despite comparable inner hair cell (IHC), IHC afferent presynaptic ribbon, and outer hair cell (OHC) densities. After noise exposure, threshold shifts were similar across genotypes, with comparable hair cell and ribbon densities across the genotypes. At one year of age, Ca<sub>V</sub>3.2 KO mice exhibited greater functional decline and OHC loss than WT and HET mice. Differences in cochlear function at 6 weeks were not explained by SGN subtype distribution or efferent terminal organization. In aged mice, mibefradil treatment reduced OHC loss but did not preserve cochlear function. These findings suggest that embryonic Ca<sub>V</sub>3.2 deletion resulted in early baseline auditory deficits, consistent with their possible developmental requirement, and did not confer protection against noise-induced or age-related hearing loss.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"135 ","pages":"Article 103138"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811520","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

The emerging role of TRPV4 in skeletal biology: Mechanotransduction, mutation, and therapeutic potential TRPV4在骨骼生物学中的新作用：机械转导、突变和治疗潜力。

IF 4 2区生物学

Cell calcium Pub Date : 2026-03-01 Epub Date: 2026-01-03 DOI: 10.1016/j.ceca.2026.103108

Bowen Lyu , Jiachen Lin , Lunhao Chen, Yue Wang

引用次数: 0

Isoform-specific structure and function of calsequestrin: Implications beyond calcium buffering in health and disease 钙栓蛋白的异构体特异性结构和功能：在健康和疾病中钙缓冲的意义

IF 4 2区生物学

Cell calcium Pub Date : 2026-03-01 Epub Date: 2026-01-11 DOI: 10.1016/j.ceca.2026.103120

Punyadhara Pani , Diya Aich , Barsha Priyadarshini Kar , M. Shiwangi Giri , Gourabamani Swalsingh , Muthu Periasamy , Naresh Chandra Bal

{"title":"Isoform-specific structure and function of calsequestrin: Implications beyond calcium buffering in health and disease","authors":"Punyadhara Pani , Diya Aich , Barsha Priyadarshini Kar , M. Shiwangi Giri , Gourabamani Swalsingh , Muthu Periasamy , Naresh Chandra Bal","doi":"10.1016/j.ceca.2026.103120","DOIUrl":"10.1016/j.ceca.2026.103120","url":null,"abstract":"<div><div>Calsequestrin (CASQ) plays an important role in muscle contraction by buffering Ca2+ inside the sarcoplasmic reticulum (SR). Intriguingly, mammals express two CASQ isoforms encoded by separate genes with highly conserved protein structure. CASQ1 is mainly expressed in fast-twitch skeletal muscles; whereas CASQ2 predominates in slow-twitch muscles and heart. CASQ2 function is poorly defined in rhythmically beating heart where SR Ca2+-release is graded through Ca2+-induced Ca2+-release (CICR), compared to CASQ1 in skeletal muscle where Ca2+-release is all or none. A unique property of CASQ is that it can dynamically polymerize-depolymerize in Ca2+-concentration dependent manner. CASQ1 and CASQ2 not only differ in their polymerization properties but also interact with different RyR protein complexes at the junctional SR governing muscle fiber specific SR Ca2+-release. In recent years CASQ has gained renewed attention because mutations in CASQ1 and CASQ2 proteins cause cardiac and skeletal muscle disease, including malignant hyperthermia (skeletal muscle), cardiac arrhythmias and sudden cardiac death. Additionally studies have implicated that CASQ is more than a Ca2+-buffer and CASQ-dysfunction can affect mitochondrial function and Ca2+-entry via store operated Ca2+-entry. Therefore, the isoform specific functions of CASQ1 and CASQ2 in different striated muscles requires further investigation in the light of recent findings. This review explores what we have learned over last 30 years about CASQ and what gaps of knowledge still exist. Here, we discuss how structural divergence between CASQ1 and CASQ2, shape physio-pathological outcomes and highlight some of the recent findings that trigger renewed interest in CASQ proteins, including their role beyond Ca2+-buffering.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"134 ","pages":"Article 103120"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145976066","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

Basic calcium phosphate crystals aggravate senescence-related osteoarthritis through GPX4-NRF2-mediated ferroptosis 碱性磷酸钙晶体通过gpx4 - nrf2介导的铁下垂加重衰老相关性骨关节炎。

IF 4 2区生物学

Cell calcium Pub Date : 2026-03-01 Epub Date: 2026-01-22 DOI: 10.1016/j.ceca.2026.103123

Yantao Zhang , Zhenxing Zhu , Piyao Ji , Yuyang Wu , Jianghua Ming , Yan Zhou

{"title":"Basic calcium phosphate crystals aggravate senescence-related osteoarthritis through GPX4-NRF2-mediated ferroptosis","authors":"Yantao Zhang , Zhenxing Zhu , Piyao Ji , Yuyang Wu , Jianghua Ming , Yan Zhou","doi":"10.1016/j.ceca.2026.103123","DOIUrl":"10.1016/j.ceca.2026.103123","url":null,"abstract":"<div><div>Osteoarthritis (OA) is a degenerative joint disorder strongly associated with senescence, involving pathological processes such as reactive oxygen species (ROS) accumulation and ferroptosis. Basic calcium phosphate (BCP) crystals are frequently found in the joints of OA patients, yet their role in OA pathogenesis remains poorly understood. Here, we aimed to investigate the role of synthetic BCP crystals in promoting OA progression and to elucidate the molecular mechanisms underlying senescence. In this study, a rat OA model was established by intra-articular injections of BCP crystals into the knee joint, and the effect of BCP crystals improving the ferroptosis phenotype of OA cartilage was investigated. Furthermore, the expression of senescence-related biomarkers and mitochondrial functions in BCP-treated chondrocytes was observed. Moreover, the role of synthetic BCP crystals in promoting ferroptosis process in chondrocytes was investigated, as well as their mechanism of action in OA, which was related to chondrocyte senescence. The <em>in vivo</em> findings demonstrated that BCP crystals accelerated cartilage senescence, worsened cartilage degradation, promoted osteophyte formation, and induced ferroptosis in the joint synovium. <em>In vitro</em>, BCP crystals intensified ferroptosis and oxidative stress in rat chondrocytes, increased ROS production, and further promoted mitochondrial dysfunction and chondrocyte senescence. Mechanistically, BCP crystals aggravated senescence-related pathological changes by inhibiting of the GPX4-NRF2 pathway and inducing ferroptosis, thereby promoting OA progression. Our findings demonstrate BCP crystals promote chondrocyte senescence by enhancing mitochondrial dysfunction and ferroptosis. This effect was mediated through downregulation of GPX4-NRF2 signaling, which provided a theoretical basis for exploring the pathogenesis and treatment of OA.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"134 ","pages":"Article 103123"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146046170","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

MONNA alleviates MPTP-induced Parkinson’s disease in zebrafish by activating TFEB dependently on ER Calcium MONNA通过依赖内质网钙激活TFEB减轻mptp诱导的斑马鱼帕金森病。

IF 4 2区生物学

Cell calcium Pub Date : 2026-03-01 Epub Date: 2026-01-30 DOI: 10.1016/j.ceca.2026.103125

Meiqin Tang , Ting Luo , Chunlan Kang , Feng Wang , Dongqing Yang , Ruili Cui , Chanjing Li , Yihan Zhang , Yiyao Liu , Min Li , Mei Hu , Ping Li

{"title":"MONNA alleviates MPTP-induced Parkinson’s disease in zebrafish by activating TFEB dependently on ER Calcium","authors":"Meiqin Tang , Ting Luo , Chunlan Kang , Feng Wang , Dongqing Yang , Ruili Cui , Chanjing Li , Yihan Zhang , Yiyao Liu , Min Li , Mei Hu , Ping Li","doi":"10.1016/j.ceca.2026.103125","DOIUrl":"10.1016/j.ceca.2026.103125","url":null,"abstract":"<div><div>A-synuclein aggregation is a biomarker of Parkinson’s disease (PD) whose feature is the progressive loss of dopaminergic neuron in the middle brain. The removal of a-synuclein aggregation through autophagy-lysosome pathway is a promising strategy for PD treatment. Transcription factor EB (TFEB) is a master regulator of autophagic and lysosomal biogenesis and function. Here, we report a library screen of intracellular Ca<sup>2+</sup> inducers to identify small-molecule agonists of TFEB and discover MONNA can promote autophagic and lysosomal activity. Notably, MONNA facilitates the reduction of pathological a-synuclein in the Parkinson’s disease model both <em>in vitro</em> and <em>in vivo</em>, and ameliorates PD-like behaviors in zebrafish. Mode of action studies reveal MONNA induces TFEB nuclear translocation through a Ca<sup>2+</sup>-dependent mechanism involving Calcineurin (CaN). Endoplasmic reticulum (ER) but not lysosome Ca<sup>2+</sup> is critical to MONNA-induced TFEB activation and autophagy induction. Furthermore, Sarcoendoplasmic reticulum calcium ATPase (SERCA) pump of ER modulates TFEB nuclear translocation induced by MONNA. Our findings demonstrate that MONNA is the first ER Ca<sup>2+</sup>-dependent small synthetic TFEB agonist promoting the degradation of a-synuclein aggregates and alleviating Parkinson’s disease. This ER Ca<sup>2+</sup>-Calcineurin-TFEB signaling pathway would broaden the way to develop drugs for PD.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"134 ","pages":"Article 103125"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118140","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

The dual role of transient receptor potential melastatin cation channels in sepsis 瞬时受体电位美伐他汀阳离子通道在脓毒症中的双重作用

IF 4 2区生物学

Cell calcium Pub Date : 2026-03-01 Epub Date: 2026-01-10 DOI: 10.1016/j.ceca.2026.103118

Jujun Liu , Qingqing Hu , Keyi Sun , Huifang Tang , Xiaowei Qian

引用次数: 0

NCKX4 regulates hippocampal Ca2+ homeostasis and contributes to contextual memory and anxiety-related behaviours NCKX4调节海马Ca2+稳态，并有助于情境记忆和焦虑相关行为。

IF 4 2区生物学

Cell calcium Pub Date : 2026-03-01 Epub Date: 2026-02-12 DOI: 10.1016/j.ceca.2026.103126

Mohamed Tarek Hassan , Guilherme Henrique Souza Bomfim , Nish Patel , Sarvan Kumar Radhakrishnan , Rodrigo S. Lacruz , Jonathan Lytton

{"title":"NCKX4 regulates hippocampal Ca2+ homeostasis and contributes to contextual memory and anxiety-related behaviours","authors":"Mohamed Tarek Hassan , Guilherme Henrique Souza Bomfim , Nish Patel , Sarvan Kumar Radhakrishnan , Rodrigo S. Lacruz , Jonathan Lytton","doi":"10.1016/j.ceca.2026.103126","DOIUrl":"10.1016/j.ceca.2026.103126","url":null,"abstract":"<div><div>The K⁺-dependent Na⁺/Ca²⁺-exchanger (NCKX) family comprises five members (NCKX1–5) that serve as key regulators of Ca²⁺ homeostasis. The fourth member, NCKX4, has been implicated in several neuronal processes, including vision, olfaction, and hypothalamic satiety signaling. We recently showed high NCKX4 expression in the mossy fibers of the hippocampus, a brain region essential for learning and memory. In this study, we investigated the impact of NCKX4 loss on Ca²⁺ dynamics in primary hippocampal neurons and assessed hippocampal-dependent behaviour in <em>Nckx4</em><sup>–/–</sup> mice. Using Ca<sup>2+</sup> imaging, we found that NCKX4 actively contributes to Ca²⁺ homeostasis in hippocampal cells and its loss is not compensated for by other Ca<sup>2+</sup> transporters. Neurons lacking NCKX4 had significantly reduced rates of total Na<sup>+</sup>/Ca<sup>2+</sup>-exchange activity and showed a decrease in the rate of Ca<sup>2+</sup> clearance following a depolarization event. Complementary behavioural testing showed deficits in contextual memory formation and recall, as well as reduced anxiety when placed in an open field, in <em>Nckx4</em><sup>–/–</sup> mice. These findings reveal a previously unrecognized role for NCKX4 in regulating hippocampal Ca<sup>2+</sup> dynamics, and support the hypothesis that NCKX4 expression is mechanistically linked to learning and memory.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"134 ","pages":"Article 103126"},"PeriodicalIF":4.0,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146225645","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: Ca2+/calmodulin-driven functions mediated by extracellular vesicles: a physiopathological perspective 对细胞外囊泡介导的Ca2+/钙调素驱动功能的更正：生理病理角度：[Cell Calcium 133(2026)103105]。

IF 4 2区生物学

Cell calcium Pub Date : 2026-03-01 Epub Date: 2026-02-06 DOI: 10.1016/j.ceca.2026.103124

Juan Alcalde , Ester Martín-Villar , Martin W. Berchtold , Antonio Villalobo

引用次数: 0