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Calcium signals as regulators of ferroptosis in cancer 钙信号是癌症中铁蛋白沉积的调节因子
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-29 DOI: 10.1016/j.ceca.2024.102966
Ioana Stejerean-Todoran , Christine S. Gibhardt , Ivan Bogeski
{"title":"Calcium signals as regulators of ferroptosis in cancer","authors":"Ioana Stejerean-Todoran ,&nbsp;Christine S. Gibhardt ,&nbsp;Ivan Bogeski","doi":"10.1016/j.ceca.2024.102966","DOIUrl":"10.1016/j.ceca.2024.102966","url":null,"abstract":"<div><div>The field of ferroptosis research has grown exponentially since this form of cell death was first identified over a decade ago. Ferroptosis, an iron- and ROS-dependent type of cell death, is controlled by various metabolic pathways, including but not limited to redox and calcium (Ca<sup>2+</sup>) homeostasis, iron fluxes, mitochondrial function and lipid metabolism. Importantly, therapy-resistant tumors are particularly susceptible to ferroptotic cell death, rendering ferroptosis a promising therapeutic strategy against numerous malignancies. Calcium signals are important regulators of both cancer progression and cell death, with recent studies indicating their involvement in ferroptosis. Cells undergoing ferroptosis are characterized by plasma membrane rupture and the formation of nanopores, which facilitate influx of ions such as Ca<sup>2+</sup> into the affected cells. Furthermore, mitochondrial Ca²⁺ levels have been implicated in directly influencing the cellular response to ferroptosis. Despite the remarkable progress made in the field, our understanding of the contribution of Ca<sup>2+</sup> signals to ferroptosis remains limited. Here, we summarize key connections between Ca²⁺ signaling and ferroptosis in cancer pathobiology and discuss their potential therapeutic significance.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102966"},"PeriodicalIF":4.3,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142586318","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
GPCR signalling: Yet another variant route in a highly complex road map GPCR 信号：高度复杂路线图中的另一条变异路线
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-24 DOI: 10.1016/j.ceca.2024.102965
Alexander Demby, Manuela Zaccolo
{"title":"GPCR signalling: Yet another variant route in a highly complex road map","authors":"Alexander Demby,&nbsp;Manuela Zaccolo","doi":"10.1016/j.ceca.2024.102965","DOIUrl":"10.1016/j.ceca.2024.102965","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102965"},"PeriodicalIF":4.3,"publicationDate":"2024-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142552072","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
Does a transmembrane sodium gradient control membrane potential in mammalian mitochondria? 跨膜钠梯度是否能控制哺乳动物线粒体的膜电位？
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-23 DOI: 10.1016/j.ceca.2024.102962
David G. Nicholls
{"title":"Does a transmembrane sodium gradient control membrane potential in mammalian mitochondria?","authors":"David G. Nicholls","doi":"10.1016/j.ceca.2024.102962","DOIUrl":"10.1016/j.ceca.2024.102962","url":null,"abstract":"<div><div>In a recent publication, Hernansanz-Agusti̒n et al. propose that a sodium gradient across the inner mitochondrial membrane, generated by a Na<sup>+</sup>/H<sup>+</sup> activity integral to Complex I can account for half of the mitochondrial membrane potential. This conflicts with conventional electrophysiological and chemiosmotic understanding.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102962"},"PeriodicalIF":4.3,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142564098","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
Calcium and chloride out of sync: The role of signaling in Sjögren's salivary gland issues 钙和氯不同步：信号在斯约格伦唾液腺问题中的作用。
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-21 DOI: 10.1016/j.ceca.2024.102964
Felipe Tribiños, Marcelo A. Catalan
{"title":"Calcium and chloride out of sync: The role of signaling in Sjögren's salivary gland issues","authors":"Felipe Tribiños,&nbsp;Marcelo A. Catalan","doi":"10.1016/j.ceca.2024.102964","DOIUrl":"10.1016/j.ceca.2024.102964","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102964"},"PeriodicalIF":4.3,"publicationDate":"2024-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495676","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 “Loss-of-function W4645R mutation in the RyR2-caffeine binding site: implications for synchrony and arrhythmogenesis” [Cell Calcium 123 (2024) 102925] RyR2-咖啡因结合位点的功能缺失W4645R突变：对同步性和心律失常发生的影响》[Cell Calcium 123 (2024) 102925]的更正。
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-20 DOI: 10.1016/j.ceca.2024.102960
José-Carlos Fernández-Morales , Noemi Toth , Pinar Bayram , Taylor Rienzo , Martin Morad
{"title":"Corrigendum to “Loss-of-function W4645R mutation in the RyR2-caffeine binding site: implications for synchrony and arrhythmogenesis” [Cell Calcium 123 (2024) 102925]","authors":"José-Carlos Fernández-Morales ,&nbsp;Noemi Toth ,&nbsp;Pinar Bayram ,&nbsp;Taylor Rienzo ,&nbsp;Martin Morad","doi":"10.1016/j.ceca.2024.102960","DOIUrl":"10.1016/j.ceca.2024.102960","url":null,"abstract":"","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102960"},"PeriodicalIF":4.3,"publicationDate":"2024-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142458791","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
ER stress as a sentinel mechanism for ER Ca2+ homeostasis ER应激是ER Ca2+平衡的哨兵机制。
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-18 DOI: 10.1016/j.ceca.2024.102961
Tadashi Makio, Junsheng Chen, Thomas Simmen
{"title":"ER stress as a sentinel mechanism for ER Ca2+ homeostasis","authors":"Tadashi Makio,&nbsp;Junsheng Chen,&nbsp;Thomas Simmen","doi":"10.1016/j.ceca.2024.102961","DOIUrl":"10.1016/j.ceca.2024.102961","url":null,"abstract":"<div><div>Endoplasmic reticulum (ER) stress is triggered upon the interference with oxidative protein folding that aims to produce fully folded, disulfide-bonded and glycosylated proteins, which are then competent to exit the ER. Many of the enzymes catalyzing this process require the binding of Ca<sup>2+</sup> ions, including the chaperones BiP/GRP78, calnexin and calreticulin. The induction of ER stress with a variety of drugs interferes with chaperone Ca<sup>2+</sup> binding, increases cytosolic Ca<sup>2+</sup>through the opening of ER Ca<sup>2+</sup> channels, and activates store-operated Ca<sup>2+</sup> entry (SOCE). Posttranslational modifications (PTMs) of the ER Ca<sup>2+</sup> handling proteins through ER stress-dependent phosphorylation or oxidation control these mechanisms, as demonstrated in the case of the sarco/endoplasmic reticulum ATPase (SERCA), inositol 1,4,5 trisphosphate receptors (IP<sub>3</sub>Rs) or stromal interaction molecule 1 (STIM1). Their aim is to restore ER Ca<sup>2+</sup> homeostasis but also to increase Ca<sup>2+</sup> transfer from the ER to mitochondria during ER stress. This latter function boosts ER bioenergetics, but also triggers apoptosis if ER Ca<sup>2+</sup> signaling persists. ER Ca<sup>2+</sup> toolkit oxidative modifications upon ER stress can occur within the ER lumen or in the adjacent cytosol. Enzymes involved in this redox control include ER oxidoreductin 1 (ERO1) or the thioredoxin-family protein disulfide isomerases (PDI) and ERp57. A tight, but adaptive connection between ER Ca<sup>2+</sup> content, ER stress and mitochondrial readouts allows for the proper functioning of many tissues, including skeletal muscle, the liver, and the pancreas, where ER stress either maintains or compromises their function, depending on its extent and context. Upon mutation of key regulators of ER Ca<sup>2+</sup> signaling, diseases such as muscular defects (e.g., from mutated selenoprotein N, SEPN1/SELENON), or diabetes (e.g., from mutated PERK) are the result.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102961"},"PeriodicalIF":4.3,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142544020","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 IP3 receptor-KRAP complex at the desmosomes: A new player in the apoptotic process 脱粘体上的 IP3 受体-KRAP 复合物：凋亡过程中的新角色
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-18 DOI: 10.1016/j.ceca.2024.102963
Jan B. Parys
{"title":"The IP3 receptor-KRAP complex at the desmosomes: A new player in the apoptotic process","authors":"Jan B. Parys","doi":"10.1016/j.ceca.2024.102963","DOIUrl":"10.1016/j.ceca.2024.102963","url":null,"abstract":"<div><div>The IP<sub>3</sub> receptor (IP<sub>3</sub>R) is a ubiquitously expressed Ca<sup>2+</sup>-release channel located in the endoplasmic reticulum (ER). Ca<sup>2+</sup> signals originating from the IP<sub>3</sub>R initiate or regulate a plethora of cellular events, including cell life and death processes, e.g. exaggerated Ca<sup>2+</sup> release from the ER to the mitochondria is a trigger for apoptosis. Recently, Cho et al. (Current Biology, 2024, DOI: 10.1016/j.cub.2024.08.057) demonstrated that in epithelial monolayers a sustained [Ca<sup>2+</sup>] elevation caused by the IP<sub>3</sub>Rs is responsible for the extrusion of adjacent apoptotic cells out of the epithelial monolayer. Interestingly, the IP<sub>3</sub>Rs involved are associated with the desmosomes via K-Ras-induced actin-interacting protein (KRAP). This study not only highlight a novel role of the IP<sub>3</sub>R in apoptosis, but also shed a new light on how KRAP -and by extension KRAP-related proteins- contribute to the regulation of IP<sub>3</sub>R activity and, more broadly, underscores the crucial role of associated proteins in determining the function of IP<sub>3</sub>Rs.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102963"},"PeriodicalIF":4.3,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142495677","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
MICU1 and MICU2, two peas in a pod or entirely different fruits? MICU1 和 MICU2 是一个豆荚里的两颗豆子，还是完全不同的果实？
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-08 DOI: 10.1016/j.ceca.2024.102959
Jiuzhou Huo, Jeffery D. Molkentin
{"title":"MICU1 and MICU2, two peas in a pod or entirely different fruits?","authors":"Jiuzhou Huo,&nbsp;Jeffery D. Molkentin","doi":"10.1016/j.ceca.2024.102959","DOIUrl":"10.1016/j.ceca.2024.102959","url":null,"abstract":"<div><div>Fluctuations in mitochondrial matrix Ca<sup>2+</sup> plays a critical role in matching energy production to cellular demand through direct effects on oxidative phosphorylation and ATP production. Disruption in mitochondrial Ca<sup>2+</sup> homeostasis, particularly under pathological conditions such as ischemia or heart failure, can lead to mitochondrial dysfunction, energy deficit, and eventually death of cardiomyocytes. The primary channel regulating acute mitochondrial Ca<sup>2+</sup> influx is the mitochondrial Ca<sup>2+</sup> uniporter (mtCU), which is regulated by the mitochondrial Ca<sup>2+</sup> uptake (MICU) proteins that were examined here.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102959"},"PeriodicalIF":4.3,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142433063","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 intricacies of mitochondrial calcium and enzyme regulation in liver metabolism 肝脏代谢中线粒体钙和酶调节的复杂性。
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-10-05 DOI: 10.1016/j.ceca.2024.102958
Cristina Mammucari
{"title":"The intricacies of mitochondrial calcium and enzyme regulation in liver metabolism","authors":"Cristina Mammucari","doi":"10.1016/j.ceca.2024.102958","DOIUrl":"10.1016/j.ceca.2024.102958","url":null,"abstract":"<div><div>Mitochondrial Ca<sup>2+</sup> plays a positive role in regulating pyruvate dehydrogenase, as well as the TCA cycle enzymes isocitrate dehydrogenase and α-ketoglutarate dehydrogenase. This regulation boosts the production of reducing equivalents that fuel the electron transport chain, ultimately driving ATP production. The Mitochondrial Calcium Uniporter (MCU) is the highly selective channel responsible for mitochondrial Ca<sup>2+</sup> uptake when local Ca<sup>2+</sup> levels reach the threshold for channel activation. In a recent study, LaMoia et al. used an innovative [<sup>13</sup>C<sub>5</sub>]glutamine-based metabolic flux analysis method (Q-flux) to measure in vivo hepatic metabolic fluxes in liver-specific MCU<sup>-/-</sup> mice. Surprisingly, they observed increased flux through isocitrate dehydrogenase and α-ketoglutarate dehydrogenase. Metabolic pathways are continuously reorganized in response to intrinsic cellular signals, as well as hormonal and nutritional inputs. Integrating metabolic flux analysis into complex systems can provide deeper insights into how metabolic adaptations occur under different conditions.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102958"},"PeriodicalIF":4.3,"publicationDate":"2024-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142406164","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
Inhibition of TRPV1 by an antagonist in clinical trials is dependent on cholesterol binding 临床试验中的拮抗剂对 TRPV1 的抑制依赖于胆固醇的结合。
IF 4.3 2区 生物学
Cell calcium Pub Date : 2024-09-25 DOI: 10.1016/j.ceca.2024.102957
Tal Brandwine-Shemmer , Baruch Minke , Irena Levitan
{"title":"Inhibition of TRPV1 by an antagonist in clinical trials is dependent on cholesterol binding","authors":"Tal Brandwine-Shemmer ,&nbsp;Baruch Minke ,&nbsp;Irena Levitan","doi":"10.1016/j.ceca.2024.102957","DOIUrl":"10.1016/j.ceca.2024.102957","url":null,"abstract":"<div><div>TRP Vanilloid 1 (TRPV1) channel, one of the major members of the TRP family was discovered to play a critical role in pain sensation, particularly inflammatory pain, and is associated with hyperalgesia, an enhanced sensitivity to pain. A new study by <em><u>Fan</u></em> <u>et al.</u> <em><u>“</u><u>Structural basis of TRPV1 inhibition by SAF312 and cholesterol</u></em>” sheds new light on the mechanistic structural basis of TRPV1 inhibition by SAF312 (Libvatrep), a TRPV1 antagonist, currently in phase II clinical trials. They discover that the binding site of SAF312 in TRPV1 is in close vicinity and partially overlaps with the binding site of cholesterol and that removal of cholesterol interferes with the ability of SAF312 to suppress TRPV1 current.</div></div>","PeriodicalId":9678,"journal":{"name":"Cell calcium","volume":"124 ","pages":"Article 102957"},"PeriodicalIF":4.3,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142364555","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
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