bims-mionch Biomed News
on Mitochondrial ion channels
Issue of 2024–03–24
nineteen papers selected by
Gun Kim, Seoul National University
  1. Detection of Nanoparticle-Mediated Change in Mitochondrial Membrane Potential in T Cells Using JC-1 Dye.
  2. Interplay of mitochondria associated membrane proteins and autophagy: Implications in neurodegeneration.
  3. Cell type-specific regulation of CFTR trafficking-on the verge of progress.
  4. Ruthenium red: Blocker or antagonist of TRPV channels?
  5. Is There a Mitochondrial Protection via Remote Ischemic Conditioning in Settings of Anticancer Therapy Cardiotoxicity?
  6. A partial Drp1 knockout improves autophagy flux independent of mitochondrial function.
  7. Dysregulation of calcium homeostasis in cancer and its role in chemoresistance.
  8. Chloroplast ion homeostasis - what do we know and where should we go?
  9. Future perspectives on the roles of mitochondrial dynamics in the heart in obesity and aging.
  10. Matrine attenuating cardiomyocyte apoptosis in doxorubicin-induced cardiotoxicity through improved mitochondrial membrane potential and activation of mitochondrial respiratory chain Complex I pathway.
  11. Targeting NAD+ Metabolism to Modulate Autoimmunity and Inflammation.
  12. Imaging Amyloid-β Membrane Interactions: Ion-Channel Pores and Lipid-Bilayer Permeability in Alzheimer's Disease.
  13. Steady-state and time-resolved fluorescent methodologies to characterize the conformational landscape of the selectivity filter of K+ channels.
  14. The phospholipids cardiolipin and phosphatidylethanolamine differentially regulate MDC biogenesis.
  15. ER-organelle contacts: A signaling hub for neurological diseases.
  16. Mitochondria-lysosome-extracellular vesicles axis and nanotheranostics in neurodegenerative diseases.
  17. The association between ferroptosis and autophagy in cardiovascular diseases.
  18. The Chemical Reactivity of Membrane Lipids.
  19. Isolation of Cytosolic Ribosomes Associated with Plant Mitochondria and Chloroplasts.
  1. Methods Mol Biol. 2024 ;2789 153-159
    Detection of Nanoparticle-Mediated Change in Mitochondrial Membrane Potential in T Cells Using JC-1 Dye.
    Ankit Shah, Marina A Dobrovolskaia.
      Alterations in mitochondrial membrane potential are associated with the generation of reactive oxygen species and cell death. While eliminating cancer cells is beneficial for cancer therapy, cytotoxicity to healthy cells may limit the therapeutic applications of mitochondria-damaging nanoparticles. Due to the critical role mitochondria play in cell viability and function, it is important to detect such alterations when studying nanomaterials for therapeutic applications. The protocol described herein utilizes JC-1 dye to detect nanoparticle-mediated changes in mitochondrial membrane potential and is intended to support mechanistic immunotoxicology studies.
    Keywords:  Membrane potential; Mitochondria; Nanoparticles; Oxidative stress; T cells
    DOI:  https://doi.org/10.1007/978-1-0716-3786-9_16
  2. Mitochondrion. 2024 Mar 19. pii: S1567-7249(24)00032-1. [Epub ahead of print] 101874
    Interplay of mitochondria associated membrane proteins and autophagy: Implications in neurodegeneration.
    Prakash G Kulkarni, Vaibhavi M Mohire, Pranjal P Waghmare, Tanushree Banerjee.
      Since the discovery of membrane contact sites between ER and mitochondria called mitochondria-associated membranes (MAMs), several pieces of evidence identified their role in the regulation of different cellular processes such as Ca2+ signalling, mitochondrial transport, and dynamics, ER stress, inflammation, glucose homeostasis, and autophagy. The integrity of these membranes was found to be essential for the maintenance of these cellular functions. Accumulating pieces of evidence suggest that MAMs serve as a platform for autophagosome formation. However, the alteration within MAMs' structure is associated with the progression of neurodegenerative diseases. Dysregulated autophagy is a hallmark of neurodegeneration. Here, in this review, we highlight the present knowledge on MAMs, their structural composition, and their roles in different cellular functions. We also discuss the association of MAMs proteins with impaired autophagy and their involvement in the progression of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
    Keywords:  Alzheimer’s disease (AD); Autophagy; Mitochondrial associated membranes (MAMs); Mitophagy; Parkinson’s disease (PD)
    DOI:  https://doi.org/10.1016/j.mito.2024.101874
  3. Front Cell Dev Biol. 2024 ;12 1338892
    Cell type-specific regulation of CFTR trafficking-on the verge of progress.
    Carlos M Farinha, Lúcia Santos, João F Ferreira.
      Trafficking of the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) protein is a complex process that starts with its biosynthesis and folding in the endoplasmic reticulum. Exit from the endoplasmic reticulum (ER) is coupled with the acquisition of a compact structure that can be processed and traffic through the secretory pathway. Once reaching its final destination-the plasma membrane, CFTR stability is regulated through interaction with multiple protein partners that are involved in its post-translation modification, connecting the channel to several signaling pathways. The complexity of the process is further boosted when analyzed in the context of the airway epithelium. Recent advances have characterized in detail the different cell types that compose the surface epithelium and shifted the paradigm on which cells express CFTR and on their individual and combined contribution to the total expression (and function) of this chloride/bicarbonate channel. Here we review CFTR trafficking and its relationship with the knowledge on the different cell types of the airway epithelia. We explore the crosstalk between these two areas and discuss what is still to be clarified and how this can be used to develop more targeted therapies for CF.
    Keywords:  CFTR; airway epithelium; basal cells; ciliated cells; ionocytes; membrane stability; protein trafficking; secretory cells
    DOI:  https://doi.org/10.3389/fcell.2024.1338892
  4. Cell Calcium. 2024 Mar 18. pii: S0143-4160(24)00032-0. [Epub ahead of print]119 102874
    Ruthenium red: Blocker or antagonist of TRPV channels?
    Andrés Jara-Oseguera.
      Ruthenium red (RR) is a widely used inhibitor of Transient Receptor Potential (TRP) cation channels and other types of ion channels. Although RR has been generally accepted to inhibit TRP channels by physically blocking the ion permeation pathway, recent structural evidence suggests that it might also function as an antagonist, inducing conformational changes in the channel upon binding that result in closure of the pore. In a recent manuscript published in EMBO Reports, Ruth A. Pumroy and collaborators solve structures of TRPV2 and TRPV5 channels in the presence and absence of activators and RR. The data sheds light on the mechanism of inhibition by RR, while also opening new questions for further investigation.
    Keywords:  Block; Ruthenium red; TRP channels; TRPV2; TRPV5; TRPV6
    DOI:  https://doi.org/10.1016/j.ceca.2024.102874
  5. Curr Heart Fail Rep. 2024 Mar 21.
    Is There a Mitochondrial Protection via Remote Ischemic Conditioning in Settings of Anticancer Therapy Cardiotoxicity?
    Petra Kleinbongard, Ioanna Andreadou.
       PURPOSE OF REVIEW: To provide an overview of (a) protective effects on mitochondria induced by remote ischemic conditioning (RIC) and (b) mitochondrial damage caused by anticancer therapy. We then discuss the available results of studies on mitochondrial protection via RIC in anticancer therapy-induced cardiotoxicity.
    RECENT FINDINGS: In three experimental studies in healthy mice and pigs, there was a RIC-mediated protection against anthracycline-induced cardiotoxicity and there was some evidence of improved mitochondrial function with RIC. The RIC-mediated protection was not confirmed in the two available studies in cancer patients. In adult cancer patients, RIC was associated with an adverse outcome. There are no data on mitochondrial function in cancer patients. Studies in tumor-bearing animals are needed to determine whether RIC does not interfere with the anticancer properties of the drugs and whether RIC actually improves mitochondrial function, ultimately resulting in improved cardiac function.
    Keywords:  Anthracycline; Cancer-treatment; Cardioprotection; Cardiotoxicity; Mitochondria; Remote ischemic conditioning
    DOI:  https://doi.org/10.1007/s11897-024-00658-w
  6. Mol Neurodegener. 2024 Mar 19. 19(1): 26
    A partial Drp1 knockout improves autophagy flux independent of mitochondrial function.
    Rebecca Z Fan, Carolina Sportelli, Yanhao Lai, Said S Salehe, Jennifer R Pinnell, Harry J Brown, Jason R Richardson, Shouqing Luo, Kim Tieu.
       BACKGROUND: Dynamin-related protein 1 (Drp1) plays a critical role in mitochondrial dynamics. Partial inhibition of this protein is protective in experimental models of neurological disorders such as Parkinson's disease and Alzheimer's disease. The protective mechanism has been attributed primarily to improved mitochondrial function. However, the observations that Drp1 inhibition reduces protein aggregation in such neurological disorders suggest the involvement of autophagy. To investigate this potential novel protective mechanism of Drp1 inhibition, a model with impaired autophagy without mitochondrial involvement is needed.
    METHODS: We characterized the effects of manganese (Mn), which causes parkinsonian-like symptoms in humans, on autophagy and mitochondria by performing dose-response studies in two cell culture models (stable autophagy HeLa reporter cells and N27 rat immortalized dopamine neuronal cells). Mitochondrial function was assessed using the Seahorse Flux Analyzer. Autophagy flux was monitored by quantifying the number of autophagosomes and autolysosomes, as well as the levels of other autophagy proteins. To strengthen the in vitro data, multiple mouse models (autophagy reporter mice and mutant Drp1+/- mice and their wild-type littermates) were orally treated with a low chronic Mn regimen that was previously reported to increase α-synuclein aggregation and transmission via exosomes. RNAseq, laser captured microdissection, immunofluorescence, immunoblotting, stereological cell counting, and behavioural studies were used. RESULTS IN VITRO: data demonstrate that at low non-toxic concentrations, Mn impaired autophagy flux but not mitochondrial function and morphology. In the mouse midbrain, RNAseq data further confirmed autophagy pathways were dysregulated but not mitochondrial related genes. Additionally, Mn selectively impaired autophagy in the nigral dopamine neurons but not the nearby nigral GABA neurons. In cells with a partial Drp1-knockdown and Drp1+/- mice, Mn induced autophagic impairment was significantly prevented. Consistent with these observations, Mn increased the levels of proteinase-K resistant α-synuclein and Drp1-knockdown protected against this pathology.
    CONCLUSIONS: This study demonstrates that improved autophagy flux is a separate mechanism conferred by Drp1 inhibition independent of its role in mitochondrial fission. Given that impaired autophagy and mitochondrial dysfunction are two prominent features of neurodegenerative diseases, the combined protective mechanisms targeting these two pathways conferred by Drp1 inhibition make this protein an attractive therapeutic target.
    Keywords:  Autophagy; Dynamin related protein 1; Manganese; Mitochondrial dynamics; Mitochondrial dysfunction; Parkinson’s disease; Protein aggregation; α-synuclein
    DOI:  https://doi.org/10.1186/s13024-024-00708-w
  7. Cancer Drug Resist. 2024 ;7 11
    Dysregulation of calcium homeostasis in cancer and its role in chemoresistance.
    Neema Kumari, Narasimha Pullaguri, Subha Narayan Rath, Ashish Bajaj, Vikas Sahu, Kranti Kiran Reddy Ealla.
      Globally, cancer, as a major public health concern, poses a severe threat to people's well-being. Advanced and specialized therapies can now cure the majority of people with early-stage cancer. However, emerging resistance to traditional and novel chemotherapeutic drugs remains a serious issue in clinical medicine. Chemoresistance often leads to cancer recurrence, metastasis, and increased mortality, accounting for 90% of chemotherapy failures. Thus, it is important to understand the molecular mechanisms of chemoresistance and find novel therapeutic approaches for cancer treatment. Among the several factors responsible for chemoresistance, calcium (Ca2+) dysregulation plays a significant role in cancer progression and chemoresistance. Therefore, targeting this derailed Ca2+ signalling for cancer therapy has become an emerging research area. Of note, the Ca2+ signal and its proteins are a multifaceted and potent tool by which cells achieve specific outcomes. Depending on cell survival needs, Ca2+ is either upregulated or downregulated in both chemosensitive and chemoresistant cancer cells. Consequently, the appropriate treatment should be selected based on Ca2+ signalling dysregulation. This review discusses the role of Ca2+ in cancer cells and the targeting of Ca2+ channels, pumps, and exchangers. Furthermore, we have emphasised the role of Ca2+ in chemoresistance and therapeutic strategies. In conclusion, targeting Ca2+ signalling is a multifaceted process. Methods such as site-specific drug delivery, target-based drug-designing, and targeting two or more Ca2+ proteins simultaneously may be explored; however, further clinical studies are essential to validate Ca2+ blockers' anti-cancer efficacy.
    Keywords:  Calcium; apoptosis; calcium channels; cancer; chemoresistance; exosome; multidrug resistance
    DOI:  https://doi.org/10.20517/cdr.2023.145
  8. New Phytol. 2024 Mar 21.
    Chloroplast ion homeostasis - what do we know and where should we go?
    Hans-Henning Kunz, Ute Armbruster, Susanne Mühlbauer, Jan de Vries, Geoffry A Davis.
      Plant yields heavily depend on proper macro- and micronutrient supply from the soil. In the leaf cells, nutrient ions fulfill specific roles in biochemical reactions, especially photosynthesis housed in the chloroplast. Here, a well-balanced ion homeostasis is maintained by a number of ion transport proteins embedded in the envelope and thylakoid membranes. Ten years ago, the first alkali metal transporters from the K+ EFFLUX ANTIPORTER family were discovered in the model plant Arabidopsis. Since then, our knowledge about the physiological importance of these carriers and their substrates has greatly expanded. New insights into the role of alkali ions in plastid gene expression and photoprotective mechanisms, both prerequisites for plant productivity in natural environments, were gained. The discovery of a Cl- channel in the thylakoid and several additional plastid alkali and alkali metal transport proteins have advanced the field further. Nevertheless, scientists still have long ways to go before a complete systemic understanding of the chloroplast's ion transportome will emerge. In this Tansley review, we highlight and discuss the achievements of the last decade. More importantly, we make recommendations on what areas to prioritize, so the field can reach the next milestones. One area, laid bare by our similarity-based comparisons among phototrophs is our lack of knowledge what ion transporters are used by cyanobacteria to buffer photosynthesis fluctuations.
    Keywords:  chloroplast; energy storage; evolution; ion transport; photosynthesis
    DOI:  https://doi.org/10.1111/nph.19661
  9. Life Sci. 2024 Mar 14. pii: S0024-3205(24)00164-4. [Epub ahead of print]344 122575
    Future perspectives on the roles of mitochondrial dynamics in the heart in obesity and aging.
    Chayodom Maneechote, Siriporn C Chattipakorn, Nipon Chattipakorn.
      Increasing global obesity rates and an aging population are independently linked to cardiac complications. Consequently, it is crucial to comprehensively understand the mechanisms behind these conditions to advance innovative therapies for age-related diseases. Mitochondrial dysfunction, specifically defects in mitochondrial fission/fusion processes, has emerged as a central regulator of cardiac complications in aging and age-related diseases (e.g., obesity). Since excessive fission and impaired fusion of cardiac mitochondria lead to disruptions in mitochondrial dynamics and cellular metabolism in aging and obesity, modulating mitochondrial dynamics with either fission inhibitors or fusion promoters has offered cardioprotection against these pathological conditions in preclinical models. This review explores the molecular mechanisms governing mitochondrial dynamics as well as the disturbances observed in aging and obesity. Additionally, pharmaceutical interventions that specifically target the processes of mitochondrial fission and fusion are presented and discussed. By establishing a connection between mitochondrial dynamism through fission and fusion and the advancement or mitigation of age-related diseases, particularly obesity, this review provides valuable insights into the progression and potential prevention strategies for such conditions.
    Keywords:  Aging; Cardiovascular disease; Mitochondria; Mitochondrial dynamics; Obesity
    DOI:  https://doi.org/10.1016/j.lfs.2024.122575
  10. Biomed Pharmacother. 2024 Mar 18. pii: S0753-3322(24)00348-2. [Epub ahead of print]173 116464
    Matrine attenuating cardiomyocyte apoptosis in doxorubicin-induced cardiotoxicity through improved mitochondrial membrane potential and activation of mitochondrial respiratory chain Complex I pathway.
    Chu Erfu, Liu Li, Qu Weiting, Chi Tao, Ma Liwei, Yang Hemin, Lu Junkun.
      The study aimed to demonstrate that matrine can reduce apoptosis in H9c2 cells induced by the cardiotoxic anticancer drug doxorubicin (DOX).The researchers pretreated H9c2 cells with different concentrations of matrine before exposing them to DOX and cultured them for 24 h. They assessed cell survival rates using cell counting kit-8 and MTT assay. Hoechst 33258 dye kits were used to determine apoptosis, while laser confocal JC-1 method was applied to test the mitochondrial membrane potential (MMP). Complex I activities were detected following the manufacturer's protocol. The results indicated that matrine pretreatment significantly increased the survival rate of H9c2 cells injured by DOX. Additionally, matrine reduced apoptosis in H9c2 cells through the improvement of MMP and activity of Complex I, which were damaged by DOX.
    Keywords:  Apoptosis; Complex I; Doxorubicin; MMP; Matrine
    DOI:  https://doi.org/10.1016/j.biopha.2024.116464
  11. J Immunol. 2024 Apr 01. 212(7): 1043-1050
    Targeting NAD+ Metabolism to Modulate Autoimmunity and Inflammation.
    Jing Wu, Kim Han, Michael N Sack.
      NAD+ biology is involved in controlling redox balance, functioning as a coenzyme in numerous enzymatic reactions, and is a cofactor for Sirtuin enzymes and a substrate for multiple regulatory enzyme reactions within and outside the cell. At the same time, NAD+ levels are diminished with aging and are consumed during the development of inflammatory and autoimmune diseases linked to aberrant immune activation. Direct NAD+ augmentation via the NAD+ salvage and Priess-Handler pathways is being investigated as a putative therapeutic intervention to improve the healthspan in inflammation-linked diseases. In this review, we survey NAD+ biology and its pivotal roles in the regulation of immunity and inflammation. Furthermore, we discuss emerging studies evaluate NAD+ boosting in murine models and in human diseases, and we highlight areas of research that remain unresolved in understanding the mechanisms of action of these nutritional supplementation strategies.
    DOI:  https://doi.org/10.4049/jimmunol.2300693
  12. Angew Chem Weinheim Bergstr Ger. 2023 Jun 19. 135(25): e202215785
    Imaging Amyloid-β Membrane Interactions: Ion-Channel Pores and Lipid-Bilayer Permeability in Alzheimer's Disease.
    John H Viles.
      The accumulation of the amyloid-β peptides (Aβ) is central to the development of Alzheimer's disease. The mechanism by which Aβ triggers a cascade of events that leads to dementia is a topic of intense investigation. Aβ self-associates into a series of complex assemblies with different structural and biophysical properties. It is the interaction of these oligomeric, protofibril and fibrillar assemblies with lipid membranes, or with membrane receptors, that results in membrane permeability and loss of cellular homeostasis, a key event in Alzheimer's disease pathology. Aβ can have an array of impacts on lipid membranes, reports have included: a carpeting effect; a detergent effect; and Aβ ion-channel pore formation. Recent advances imaging these interactions are providing a clearer picture of Aβ induced membrane disruption. Understanding the relationship between different Aβ structures and membrane permeability will inform therapeutics targeting Aβ cytotoxicity.
    Keywords:  Amyloid; Annular Oligomers; Electron Microscopy; Protofibrils; Structure
    DOI:  https://doi.org/10.1002/ange.202215785
  13. Methods. 2024 Mar 18. pii: S1046-2023(24)00079-3. [Epub ahead of print]
    Steady-state and time-resolved fluorescent methodologies to characterize the conformational landscape of the selectivity filter of K+ channels.
    María Lourdes Renart, Ana Marcela Giudici, José M González-Ros, José A Poveda.
      A variety of equilibrium and non-equilibrium methods have been used in a multidisciplinary approach to study the conformational landscape associated with the binding of different cations to the pore of potassium channels. These binding processes, and the conformational changes resulting therefrom, modulate the functional properties of such integral membrane properties, revealing these permeant and blocking cations as true effectors of such integral membrane proteins. KcsA, a prototypic K+ channel from Streptomyces lividans, has been extensively characterized in this regard. Here, we revise several fluorescence-based approaches to monitor cation binding under different experimental conditions in diluted samples, analyzing the advantages and disadvantages of each approach. These studies have contributed to explain the selectivity, conduction, and inactivation properties of K+ channels at the molecular level, together with the allosteric communication between the two gates that control the ion channel flux, and how they are modulated by lipids.
    Keywords:  Anisotropy; Fluorescence spectroscopy; Homo-FRET; Ion binding; KcsA; Potassium channels; Selectivity filter; Thermal denaturation
    DOI:  https://doi.org/10.1016/j.ymeth.2024.02.010
  14. J Cell Biol. 2024 May 06. pii: e202302069. [Epub ahead of print]223(5):
    The phospholipids cardiolipin and phosphatidylethanolamine differentially regulate MDC biogenesis.
    Tianyao Xiao, Alyssa M English, Zachary N Wilson, J Alan Maschek, James E Cox, Adam L Hughes.
      Cells utilize multiple mechanisms to maintain mitochondrial homeostasis. We recently characterized a pathway that remodels mitochondria in response to metabolic alterations and protein overload stress. This remodeling occurs via the formation of large membranous structures from the mitochondrial outer membrane called mitochondrial-derived compartments (MDCs), which are eventually released from mitochondria and degraded. Here, we conducted a microscopy-based screen in budding yeast to identify factors that regulate MDC formation. We found that two phospholipids, cardiolipin (CL) and phosphatidylethanolamine (PE), differentially regulate MDC biogenesis. CL depletion impairs MDC biogenesis, whereas blocking mitochondrial PE production leads to constitutive MDC formation. Additionally, in response to metabolic MDC activators, cellular and mitochondrial PE declines, and overexpressing mitochondrial PE synthesis enzymes suppress MDC biogenesis. Altogether, our data indicate a requirement for CL in MDC biogenesis and suggest that PE depletion may stimulate MDC formation downstream of MDC-inducing metabolic stress.
    DOI:  https://doi.org/10.1083/jcb.202302069
  15. Pharmacol Res. 2024 Mar 20. pii: S1043-6618(24)00093-8. [Epub ahead of print] 107149
    ER-organelle contacts: A signaling hub for neurological diseases.
    Yunli Wang, Jinghua Yang.
      Neuronal health is closely linked to the homeostasis of intracellular organelles, and organelle dysfunction affects the pathological progression of neurological diseases. In contrast to isolated cellular compartments, a growing number of studies have found that organelles are largely interdependent structures capable of communicating through membrane contact sites (MCSs). MCSs have been identified as key pathways mediating inter-organelle communication crosstalk in neurons, and their alterations have been linked to neurological disease pathology. The endoplasmic reticulum (ER) is a membrane-bound organelle capable of forming an extensive network of pools and tubules with important physiological functions within neurons. There are multiple MCSs between the ER and other organelles and the plasma membrane (PM), which regulate a variety of cellular processes. In this review, we focus on ER-organelle MCSs and their role in a variety of neurological diseases. We compared the biological effects between different tethering proteins and the effects of their respective disease counterparts. We also discuss how altered ER-organelle contacts may affect disease pathogenesis. Therefore, understanding the molecular mechanisms of ER-organelle MCSs in neuronal homeostasis will lay the foundation for the development of new therapies targeting ER-organelle contacts.
    Keywords:  ER-organelle crosstalk; MCSs; neurodegeneration; neurological disorders; tethering proteins
    DOI:  https://doi.org/10.1016/j.phrs.2024.107149
  16. Exp Neurol. 2024 Mar 18. pii: S0014-4886(24)00083-9. [Epub ahead of print]376 114757
    Mitochondria-lysosome-extracellular vesicles axis and nanotheranostics in neurodegenerative diseases.
    Liang Kou, Yiming Wang, Jingwen Li, Wenkai Zou, Zongjie Jin, Sijia Yin, Xiaosa Chi, Yadi Sun, Jiawei Wu, Tao Wang, Yun Xia.
      The intricate functional interactions between mitochondria and lysosomes play a pivotal role in maintaining cellular homeostasis and proper cellular functions. This dynamic interplay involves the exchange of molecules and signaling, impacting cellular metabolism, mitophagy, organellar dynamics, and cellular responses to stress. Dysregulation of these processes has been implicated in various neurodegenerative diseases. Additionally, mitochondrial-lysosomal crosstalk regulates the exosome release in neurons and glial cells. Under stress conditions, neurons and glial cells exhibit mitochondrial dysfunction and a fragmented network, which further leads to lysosomal dysfunction, thereby inhibiting autophagic flux and enhancing exosome release. This comprehensive review synthesizes current knowledge on mitochondrial regulation of cell death, organelle dynamics, and vesicle trafficking, emphasizing their significant contributions to neurodegenerative diseases. Furthermore, we explore the emerging field of nanomedicine in the management of neurodegenerative diseases. The review provides readers with an insightful overview of nano strategies that are currently advancing the mitochondrial-lysosome-extracellular vesicle axis as a therapeutic approach for mitigating neurodegenerative diseases.
    Keywords:  Extracellular vesicles axis; Lysosome; Mitochondria; Nanotheranostics; Neurodegenerative diseases
    DOI:  https://doi.org/10.1016/j.expneurol.2024.114757
  17. Cell Biochem Funct. 2024 Mar;42(2): e3985
    The association between ferroptosis and autophagy in cardiovascular diseases.
    Yifan Zhang, Junjun Yang, Chenxi Ouyang, Ning Meng.
      Autophagy is a process in which cells degrade intracellular substances and play a variety of roles in cells, such as maintaining intracellular homeostasis, preventing cell overgrowth, and removing pathogens. It is highly conserved during the evolution of eukaryotic cells. So far, the study of autophagy is still a hot topic in the field of cytology. Ferroptosis is an iron-dependent form of cell death, accompanied by the accumulation of reactive oxygen species and lipid peroxides. With the deepening of research, it has been found that ferroptosis, like autophagy, is involved in the occurrence and development of cardiovascular diseases. The relationship between autophagy and ferroptosis is complex, and the association between the two in cardiovascular disease remains to be clarified. This article reviews the mechanism of autophagy and ferroptosis and their correlation, and discusses the relationship between them in cardiovascular diseases, which is expected to provide new and important treatment strategies for cardiovascular diseases.
    Keywords:  autophagy; cardiovascular disease; cytoplasm; ferroptosis; lipid peroxide
    DOI:  https://doi.org/10.1002/cbf.3985
  18. Chem Rev. 2024 Mar 18.
    The Chemical Reactivity of Membrane Lipids.
    Genevieve Duché, John M Sanderson.
      It is well-known that aqueous dispersions of phospholipids spontaneously assemble into bilayer structures. These structures have numerous applications across chemistry and materials science and form the fundamental structural unit of the biological membrane. The particular environment of the lipid bilayer, with a water-poor low dielectric core surrounded by a more polar and better hydrated interfacial region, gives the membrane particular biophysical and physicochemical properties and presents a unique environment for chemical reactions to occur. Many different types of molecule spanning a range of sizes, from dissolved gases through small organics to proteins, are able to interact with membranes and promote chemical changes to lipids that subsequently affect the physicochemical properties of the bilayer. This Review describes the chemical reactivity exhibited by lipids in their membrane form, with an emphasis on conditions where the lipids are well hydrated in the form of bilayers. Key topics include the following: lytic reactions of glyceryl esters, including hydrolysis, aminolysis, and transesterification; oxidation reactions of alkenes in unsaturated fatty acids and sterols, including autoxidation and oxidation by singlet oxygen; reactivity of headgroups, particularly with reactive carbonyl species; and E/Z isomerization of alkenes. The consequences of reactivity for biological activity and biophysical properties are also discussed.
    DOI:  https://doi.org/10.1021/acs.chemrev.3c00608
  19. Methods Mol Biol. 2024 ;2776 289-302
    Isolation of Cytosolic Ribosomes Associated with Plant Mitochondria and Chloroplasts.
    Laura Dimnet, Thalia Salinas-Giegé, Sara Pullara, Lucas Moyet, Chloé Genevey, Marcel Kuntz, Anne-Marie Duchêne, Norbert Rolland.
      Excluding the few dozen proteins encoded by the chloroplast and mitochondrial genomes, the majority of plant cell proteins are synthesized by cytosolic ribosomes. Most of these nuclear-encoded proteins are then targeted to specific cell compartments thanks to localization signals present in their amino acid sequence. These signals can be specific amino acid sequences known as transit peptides, or post-translational modifications, ability to interact with specific proteins or other more complex regulatory processes. Furthermore, in eukaryotic cells, protein synthesis can be regulated so that certain proteins are synthesized close to their destination site, thus enabling local protein synthesis in specific compartments of the cell. Previous studies have revealed that such locally translating cytosolic ribosomes are present in the vicinity of mitochondria and emerging views suggest that localized translation near chloroplasts could also occur. However, in higher plants, very little information is available on molecular mechanisms controlling these processes and there is a need to characterize cytosolic ribosomes associated with organelles membranes. To this goal, this protocol describes the purification of higher plant chloroplast and mitochondria and the organelle-associated cytosolic ribosomes.
    Keywords:  Chloroplast; Cytosolic ribosomes; Mitochondria; Organelle
    DOI:  https://doi.org/10.1007/978-1-0716-3726-5_18
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