International Journal of Molecular Sciences

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10 pages, 401 KiB

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Dopamine: A New Player in the Pathogenesis of Diabetic Retinopathy?

by Marianthi Ntikoudi, Theofano Myrto Farmaki and Konstantinos Tziomalos

Int. J. Mol. Sci. 2024, 25(23), 13196; https://doi.org/10.3390/ijms252313196 - 8 Dec 2024

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Diabetic retinopathy (DR) is a leading cause of blindness. The pathogenesis of diabetic retinopathy is multifactorial and incompletely understood. Accordingly, treatment options are limited. Recent data suggest that dopamine might play a role in the development and progression of DR. In the present [...] Read more.

Diabetic retinopathy (DR) is a leading cause of blindness. The pathogenesis of diabetic retinopathy is multifactorial and incompletely understood. Accordingly, treatment options are limited. Recent data suggest that dopamine might play a role in the development and progression of DR. In the present review, we discuss these data and comment on the potential role of dopamine modulation in the management of this devastating microvascular complication of diabetes mellitus. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular and Cellular Biology 2024)

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31 pages, 929 KiB

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Different Therapeutic Approaches for Dry and Wet AMD

by Nicoletta Marchesi, Martina Capierri, Alessia Pascale and Annalisa Barbieri

Int. J. Mol. Sci. 2024, 25(23), 13053; https://doi.org/10.3390/ijms252313053 - 4 Dec 2024

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Abstract

Age-related macular degeneration (AMD) is the most common cause of irreversible loss of central vision in elderly subjects, affecting men and women equally. It is a degenerative pathology that causes progressive damage to the macula, the central and most vital part of the [...] Read more.

Age-related macular degeneration (AMD) is the most common cause of irreversible loss of central vision in elderly subjects, affecting men and women equally. It is a degenerative pathology that causes progressive damage to the macula, the central and most vital part of the retina. There are two forms of AMD depending on how the macula is damaged, dry AMD and wet or neovascular AMD. Dry AMD is the most common form; waste materials accumulate under the retina as old cells die, not being replaced. Wet AMD is less common, but can lead to vision loss much more quickly. Wet AMD is characterized by new abnormal blood vessels developing under the macula, where they do not normally grow. This frequently occurs in patients who already have dry AMD, as new blood vessels are developed to try to solve the problem. It is not known what causes AMD to develop; however, certain risk factors (i.e., age, smoking, genetic factors) can increase the risk of developing AMD. There are currently no treatments for dry AMD. There is evidence that not smoking, exercising regularly, eating nutritious food, and taking certain supplements can reduce the risk of acquiring AMD or slow its development. The main treatment for wet AMD is inhibitors of VEGF (vascular endothelial growth factor), a protein that stimulates the growth of new blood vessels. VEGF inhibitors can stop the growth of new blood vessels, preventing further damage to the macula and vision loss. In most patients, VEGF inhibitors can improve vision if macular degeneration is diagnosed early and treated accordingly. However, VEGF inhibitors cannot repair damage that has already occurred. Current AMD research is trying to find treatments for dry AMD and other options for wet AMD. This review provides a summary of the current evidence regarding the different treatments aimed at both forms of AMD with particular and greater attention to the dry form. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular and Cellular Biology 2024)

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13 pages, 408 KiB

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The Ubiquinone-Ubiquinol Redox Cycle and Its Clinical Consequences: An Overview

by David Mantle, Mollie Dewsbury and Iain P. Hargreaves

Int. J. Mol. Sci. 2024, 25(12), 6765; https://doi.org/10.3390/ijms25126765 - 20 Jun 2024

Cited by 1 | Viewed by 2423

Abstract

Coenzyme Q10 (CoQ10) plays a key role in many aspects of cellular metabolism. For CoQ10 to function normally, continual interconversion between its oxidised (ubiquinone) and reduced (ubiquinol) forms is required. Given the central importance of this ubiquinone–ubiquinol redox cycle, this article reviews what [...] Read more.

Coenzyme Q10 (CoQ10) plays a key role in many aspects of cellular metabolism. For CoQ10 to function normally, continual interconversion between its oxidised (ubiquinone) and reduced (ubiquinol) forms is required. Given the central importance of this ubiquinone–ubiquinol redox cycle, this article reviews what is currently known about this process and the implications for clinical practice. In mitochondria, ubiquinone is reduced to ubiquinol by Complex I or II, Complex III (the Q cycle) re-oxidises ubiquinol to ubiquinone, and extra-mitochondrial oxidoreductase enzymes participate in the ubiquinone–ubiquinol redox cycle. In clinical terms, the outcome of deficiencies in various components associated with the ubiquinone–ubiquinol redox cycle is reviewed, with a particular focus on the potential clinical benefits of CoQ10 and selenium co-supplementation. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular and Cellular Biology 2024)

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24 pages, 3620 KiB

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Comparative Review on Cancer Pathology from Aberrant Histone Chaperone Activity

by Jiho Lee and Xiucong Bao

Int. J. Mol. Sci. 2024, 25(12), 6403; https://doi.org/10.3390/ijms25126403 - 10 Jun 2024

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Abstract

Histone chaperones are integral to chromatin dynamics, facilitating the assembly and disassembly of nucleosomes, thereby playing a crucial role in regulating gene expression and maintaining genomic stability. Moreover, they prevent aberrant histone interactions prior to chromatin assembly. Disruption in histone chaperone function may [...] Read more.

Histone chaperones are integral to chromatin dynamics, facilitating the assembly and disassembly of nucleosomes, thereby playing a crucial role in regulating gene expression and maintaining genomic stability. Moreover, they prevent aberrant histone interactions prior to chromatin assembly. Disruption in histone chaperone function may result in genomic instability, which is implicated in pathogenesis. This review aims to elucidate the role of histone chaperones in cancer pathologies and explore their potential as therapeutic targets. Histone chaperones have been found to be dysregulated in various cancers, with alterations in expression levels, mutations, or aberrant interactions leading to tumorigenesis and cancer progression. In addition, this review intends to highlight the molecular mechanisms of interactions between histone chaperones and oncogenic factors, underscoring their roles in cancer cell survival and proliferation. The dysregulation of histone chaperones is significantly correlated with cancer development, establishing them as active contributors to cancer pathology and viable targets for therapeutic intervention. This review advocates for continued research into histone chaperone-targeted therapies, which hold potential for precision medicine in oncology. Future advancements in understanding chaperone functions and interactions are anticipated to lead to novel cancer treatments, enhancing patient care and outcomes. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular and Cellular Biology 2024)

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30 pages, 1728 KiB

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Arrestins: A Small Family of Multi-Functional Proteins

by Vsevolod V. Gurevich

Int. J. Mol. Sci. 2024, 25(11), 6284; https://doi.org/10.3390/ijms25116284 - 6 Jun 2024

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Abstract

The first member of the arrestin family, visual arrestin-1, was discovered in the late 1970s. Later, the other three mammalian subtypes were identified and cloned. The first described function was regulation of G protein-coupled receptor (GPCR) signaling: arrestins bind active phosphorylated GPCRs, blocking [...] Read more.

The first member of the arrestin family, visual arrestin-1, was discovered in the late 1970s. Later, the other three mammalian subtypes were identified and cloned. The first described function was regulation of G protein-coupled receptor (GPCR) signaling: arrestins bind active phosphorylated GPCRs, blocking their coupling to G proteins. It was later discovered that receptor-bound and free arrestins interact with numerous proteins, regulating GPCR trafficking and various signaling pathways, including those that determine cell fate. Arrestins have no enzymatic activity; they function by organizing multi-protein complexes and localizing their interaction partners to particular cellular compartments. Today we understand the molecular mechanism of arrestin interactions with GPCRs better than the mechanisms underlying other functions. However, even limited knowledge enabled the construction of signaling-biased arrestin mutants and extraction of biologically active monofunctional peptides from these multifunctional proteins. Manipulation of cellular signaling with arrestin-based tools has research and likely therapeutic potential: re-engineered proteins and their parts can produce effects that conventional small-molecule drugs cannot. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular and Cellular Biology 2024)

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Functional elements of arrestins. Crystal structure of bovine arrestin-2 (PDB ID 1G4M [<a href="#B49-ijms-25-06284" class="html-bibr">49</a>]). Functional elements are indicated as follows: residues in the polar core (Asp26, Arg169, Asp290, Asp297; Arg 393 in the C-terminus is not resolved in this monomer and therefore is not shown) and three-element interaction (Val8 and Phe9 in β-strand I; Leu100, Leu104, and Leu108 in the α-helix; and Ile386, Val387, and Phe388 in the C-terminus are not resolved in the structure of this monomer and therefore are not shown) are shown as CPK models, and Lys10, Lys11, and Lys294, as well as C-edge residues 190–192 and N-edge residues 157–161 are shown as stick models. The following elements are highlighted by color: the finger loop (residues 64–74; red), the middle loop (residues 129–139; light blue), the lariat loop (residues 275–316; light red), N-edge (residues 157–161; orange), C-edge (residues 190–192; pink; note that the other C-edge loop, residues 334–338, is not shown because it is not resolved in the structure of this monomer), and inter-domain hinge region (residues 173–184; yellow). The chemical nature of the modeled residues is shown, as follows: hydrophobic, yellow; positively charged, dark blue; negatively charged, bright red. Image was created in DS ViewerPro 6.0 (Dassault Systèmes, San Diego, CA, USA). Full article ">Figure 2
Binding selectivity of arrestins. The binding of arrestin-1 to rhodopsin, arrestin-2 to M2 muscarinic receptor (M2R), and arrestin-3 to β2-adrenergic receptor (b2AR) is shown. Functional forms of the receptors are indicated, as follows: P, inactive phosphorylated; P*, activated phosphorylated; -, inactive unphosphorylated; *, activated unphosphorylated. Full article ">Figure 3
Arrestin elements that determine receptor preference. These were identified in [<a href="#B105-ijms-25-06284" class="html-bibr">105</a>]: arrestin-1 residues 49–90 in the N-domain and 237–268 in the C-domain, and homologous arrestin-2 residues 45–86 and 233–262. The structures are shown as solid ribbons. Receptor-discriminator elements are shown in red on the structure of arrestin-1 (PDB ID 1CF1 [<a href="#B20-ijms-25-06284" class="html-bibr">20</a>]) and arrestin-2 (PDB ID 1G4M [<a href="#B49-ijms-25-06284" class="html-bibr">49</a>]). The remaining arrestin-1 and -2 molecules are shown in blue. Images were created in DS ViewerPro 6.0 (Dassault Systèmes, San Diego, CA, USA). Full article ">

22 pages, 2466 KiB

Open AccessReview

Navigating the Maze of Kinases: CaMK-like Family Protein Kinases and Their Role in Atherosclerosis

by Jules T. J. Teuwen, Emiel P. C. van der Vorst and Sanne L. Maas

Int. J. Mol. Sci. 2024, 25(11), 6213; https://doi.org/10.3390/ijms25116213 - 5 Jun 2024

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Abstract

Circulating low-density lipoprotein (LDL) levels are a major risk factor for cardiovascular diseases (CVD), and even though current treatment strategies focusing on lowering lipid levels are effective, CVD remains the primary cause of death worldwide. Atherosclerosis is the major cause of CVD and [...] Read more.

Circulating low-density lipoprotein (LDL) levels are a major risk factor for cardiovascular diseases (CVD), and even though current treatment strategies focusing on lowering lipid levels are effective, CVD remains the primary cause of death worldwide. Atherosclerosis is the major cause of CVD and is a chronic inflammatory condition in which various cell types and protein kinases play a crucial role. However, the underlying mechanisms of atherosclerosis are not entirely understood yet. Notably, protein kinases are highly druggable targets and represent, therefore, a novel way to target atherosclerosis. In this review, the potential role of the calcium/calmodulin-dependent protein kinase-like (CaMKL) family and its role in atherosclerosis will be discussed. This family consists of 12 subfamilies, among which are the well-described and conserved liver kinase B1 (LKB1) and 5′ adenosine monophosphate-activated protein kinase (AMPK) subfamilies. Interestingly, LKB1 plays a key role and is considered a master kinase within the CaMKL family. It has been shown that LKB1 signaling leads to atheroprotective effects, while, for example, members of the microtubule affinity-regulating kinase (MARK) subfamily have been described to aggravate atherosclerosis development. These observations highlight the importance of studying kinases and their signaling pathways in atherosclerosis, bringing us a step closer to unraveling the underlying mechanisms of atherosclerosis. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular and Cellular Biology 2024)

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The maze of protein kinases. (A) Classification of protein kinases according to their amino acid residue phosphorylate capacity. Within the categories, several kinase groups, families, and subfamilies can be distinguished; subdivision is based on sequence similarity between protein kinase domains. The CaMKL family (part of the CaMK group) is the focus of this review and is highlighted in orange. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a> (accessed on 3 June 2024). (B) Coral tree showing the degree of sequence similarity between protein kinases. The location of the CaMK-like family is highlighted in red. CaMK: calcium/calmodulin-dependent protein kinase group; CaMKL: calcium/calmodulin-dependent protein kinase-like family. Created with <a href="http://phanstiel-lab.med.unc.edu/CORAL/" target="_blank">phanstiel-lab.med.unc.edu/CORAL/</a> (accessed on 3 June 2024). Full article ">Figure 2
Role of AMPK in atherosclerosis. AMPK plays an anti-inflammatory role across a variety of cell types (macrophages, dendritic cells, CD4+ T cells, ECs, and VSCMCs) and thereby protects against the development of atherosclerosis. AMPK inhibits foam cell formation and promotes M2 polarization in macrophages. Additionally, AMPK reduces pro-inflammatory cytokine release and decreases the expression of costimulatory molecules in dendritic cells. Furthermore, AMPK has an anti-inflammatory role within ECs, where it inhibits NF-κB signaling as well as NLRP3 inflammasome activation whilst enhancing the barrier function of the endothelium. Finally, AMPK may promote Treg differentiation as well as inhibit VSMC phenotype switching. Arrows pointing up and down indicate an increase or decrease, respectively. AMPK: 5′-AMP-activated protein kinase catalytic; EC: endothelial cell; M2: alternatively activated macrophage; NF-κB: nuclear factor kappa B; NLRP3: nucleotide-binding oligomerization domain (NOD)-, leucine-rich repeat (LRR)-, and pyrin domain-containing protein 3; Treg: regulatory T cell; VSMC: vascular smooth muscle cell. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a> (accessed on 3 June 2024). Full article ">Figure 3
Role of LKB1 in atherosclerosis. LKB1 plays a major anti-inflammatory role across a variety of cell types (macrophages, CD4+ T cells, and VSMCs) and thereby protects from atherosclerosis development. Importantly, LKB1 inhibits foam cell formation but also inhibits NF-κB signaling as well as promotes autophagy of inflammasome components. Moreover, in CD4+ T cells, it promotes FOXP3 expression and TGF-β signaling. Finally, in VSMCs, LKB1 reduces vascular calcification. Arrows pointing up and down indicate an increase or decrease, respectively. EC: endothelial cell; FOXP3: forkhead box protein P3; LKB1: liver kinase B1; NF-κB: nuclear factor kappa B; TGF-β: transforming growth factor-beta; VSMC: vascular smooth muscle cell. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a> (accessed on 3 June 2024). Full article ">Figure 4
Role of MARK4 in atherogenic processes. MARK4 may aggravate atherosclerosis by regulating inflammasome activation, possibly via activating JNK, NF-κB signaling via its upstream kinase IKKα, and SREBP-1c signaling. Inflammasome activation and NF-κB signaling are important mediators of inflammation and are detrimental in the context of atherosclerosis. SREBP-1c signaling is involved in de novo lipogenesis. IKKα: inhibitor of κB (IκB) kinase-α; JNK: c-Jun N-terminal kinase; MARK4: microtubule affinity-regulating kinase 4; NF-κB: nuclear factor kappa B; NLRP3: nucleotide-binding oligomerization domain (NOD)-, leucine-rich repeat (LRR)- and pyrin domain-containing protein 3; SREBP-1c: sterol regulatory element-binding protein-1c. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a> (accessed on 3 June 2024). Full article ">

22 pages, 2268 KiB

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Electro-Metabolic Coupling of Cumulus–Oocyte Complex

by Diletta Del Bianco, Rosaria Gentile, Luana Sallicandro, Andrea Biagini, Paola Tiziana Quellari, Elko Gliozheni, Paola Sabbatini, Francesco Ragonese, Antonio Malvasi, Antonio D’Amato, Giorgio Maria Baldini, Giuseppe Trojano, Andrea Tinelli and Bernard Fioretti

Int. J. Mol. Sci. 2024, 25(10), 5349; https://doi.org/10.3390/ijms25105349 - 14 May 2024

Cited by 1 | Viewed by 2236

Abstract

Oocyte–cumulus cell interaction is essential for oocyte maturation and competence. The bidirectional crosstalk network mediated by gap junctions is fundamental for the metabolic cooperation between these cells. As cumulus cells exhibit a more glycolytic phenotype, they can provide metabolic substrates that the oocyte [...] Read more.

Oocyte–cumulus cell interaction is essential for oocyte maturation and competence. The bidirectional crosstalk network mediated by gap junctions is fundamental for the metabolic cooperation between these cells. As cumulus cells exhibit a more glycolytic phenotype, they can provide metabolic substrates that the oocyte can use to produce ATP via oxidative phosphorylation. The impairment of mitochondrial activity plays a crucial role in ovarian aging and, thus, in fertility, determining the success or failure of assisted reproductive techniques. This review aims to deepen the knowledge about the electro-metabolic coupling of the cumulus–oocyte complex and to hypothesize a putative role of potassium channel modulators in order to improve fertility, promote intracellular Ca²⁺ influx, and increase the mitochondrial biogenesis and resulting ATP levels in cumulus cells. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular and Cellular Biology 2024)

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Bidirectional cumulus–oocyte relationship. A model showing intercellular communication in the cumulus–oocyte complex (COC). The cellular crosstalk between the oocyte and the surrounding somatic cells is mediated by communication through gap junctions, allowing the passage of low-molecular-weight molecules. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a> (accessed on 25 January 2024). Full article ">Figure 2
Regulation of oocyte maturation. Schematic diagram of oocyte meiotic arrest in the phase preceding the gonadotropic peak (left) and gonadotropin-induced oocyte meiotic resumption (right). Meiotic regulation is modulated by the levels of cyclic guanosine monophosphate (cGMP) and Adenosine 3′,5′-cyclic monophosphate (cAMP) that are transferred from cumulus cells (CCs) to the oocyte. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a> (accessed on 25 January 2024). Full article ">Figure 3
Cumulus–oocyte metabolic coupling. Cumulus and oocyte cell metabolic reprogramming is dependent on the pyruvate dehydrogenase kinase (PDK) and pyruvate dehydrogenase (PDH) enzymes. The schematic illustration shows the molecular mechanisms of glucose metabolism within the COC. Metabolic cooperation between the two cell types is also made possible by the transfer of Adenosine triphosphate (ATP) generated by the heap via glycolysis and the adenosine salvage pathway. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a> (accessed on 25 January 2024). Full article ">Figure 4
Mitochondrial biogenesis. The schematic diagram shows how resveratrol decreases the functional expression of voltage-dependent potassium currents by causing a depolarization of the cell membrane in human ovarian granulosa cells (hGCs). This event promotes an increase in intracellular Ca2+ that leads to an improvement in mitochondrial function with an increase in mitochondrial biogenesis. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a> (accessed on 25 January 2024). Full article ">Figure 5
Role of intracellular calcium in oocyte maturation. Follicle-stimulating hormone (FSH), luteinizing hormone (LH), and epidermal growth factor-like (EGF-like) paracrine factors bind to their receptors on the cumulus cell and induce intracellular Ca mobilization. The increase of intracellular Ca2+ in the CCs can be transmitted to the oocyte through gap junctions. In the oocyte, Ca can inhibit adenylyl cyclase isoform 3 (AC3), resulting in a reduction in cAMP in the oocyte. Alternatively, Ca2+ can activate Ca/calmodulin-dependent protein kinase II (CAMKII), which in turn activates Maturation Promoting Factor (MPF) and mitogen-activated protein kinase (MAPK), promoting cell cycle progression and spindle formation important for oocyte maturation. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a>. Full article ">Figure 6
Metabolic switch in COC depending on the stage of folliculogenesis. The schematic diagram shows the metabolic switch of the COC in relation to follicle size depending on the stage of folliculogenesis. However, the metabolism of CCs is oxidative when the follicle is small and well irrigated, while it becomes glycolytic when the follicle grows and matures. Cx43 levels during the folliculogenesis indicate the formation of the maximum number of gap junctions when the follicle is mature. Created with <a href="http://BioRender.com" target="_blank">BioRender.com</a> (accessed on 25 January 2024). Full article ">

16 pages, 3079 KiB

Open AccessReview

Potential Exosome Biomarkers for Parkinson’s Disease Diagnosis: A Systematic Review and Meta-Analysis

by Ka Young Kim, Ki Young Shin and Keun-A Chang

Int. J. Mol. Sci. 2024, 25(10), 5307; https://doi.org/10.3390/ijms25105307 - 13 May 2024

Cited by 2 | Viewed by 2234

Abstract

Parkinson’s disease (PD) is the second most common neurodegenerative disease worldwide. Given its prevalence, reliable biomarkers for early diagnosis are required. Exosomal proteins within extracellular nanovesicles are promising candidates for diagnostic, screening, prognostic, and disease monitoring purposes in neurological diseases such as PD. [...] Read more.

Parkinson’s disease (PD) is the second most common neurodegenerative disease worldwide. Given its prevalence, reliable biomarkers for early diagnosis are required. Exosomal proteins within extracellular nanovesicles are promising candidates for diagnostic, screening, prognostic, and disease monitoring purposes in neurological diseases such as PD. This review aims to evaluate the potential of extracellular vesicle proteins or miRNAs as biomarkers for PD. A comprehensive literature search until January 2024 was conducted across multiple databases, including PubMed, EMBASE, Web of Science, and Cochrane Library, to identify relevant studies reporting exosome biomarkers in blood samples from PD patients. Out of 417 articles screened, 47 studies were selected for analysis. Among exosomal protein biomarkers, α-synuclein, tau, Amyloid β 1-42, and C-X-C motif chemokine ligand 12 (CXCL12) were identified as significant markers for PD. Concerning miRNA biomarkers, miRNA-24, miR-23b-3p, miR-195-3p, miR-29c, and mir-331-5p are promising across studies. α-synuclein exhibited increased levels in PD patients compared to control groups in twenty-one studies, while a decrease was observed in three studies. Our meta-analysis revealed a significant difference in total exosomal α-synuclein levels between PD patients and healthy controls (standardized mean difference [SMD] = 1.369, 95% confidence interval [CI] = 0.893 to 1.846, p < 0.001), although these results are limited by data availability. Furthermore, α-synuclein levels significantly differ between PD patients and healthy controls (SMD = 1.471, 95% CI = 0.941 to 2.002, p < 0.001). In conclusion, certain exosomal proteins and multiple miRNAs could serve as potential biomarkers for diagnosis, prognosis prediction, and assessment of disease progression in PD. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular and Cellular Biology 2024)

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15 pages, 560 KiB

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Essential Role of Astrocytes in Learning and Memory

by Paula Escalada, Amaia Ezkurdia, María Javier Ramírez and Maite Solas

Int. J. Mol. Sci. 2024, 25(3), 1899; https://doi.org/10.3390/ijms25031899 - 5 Feb 2024

Cited by 9 | Viewed by 7457

Abstract

One of the most biologically relevant functions of astrocytes within the CNS is the regulation of synaptic transmission, i.e., the physiological basis for information transmission between neurons. Changes in the strength of synaptic connections are indeed thought to be the cellular basis of [...] Read more.

One of the most biologically relevant functions of astrocytes within the CNS is the regulation of synaptic transmission, i.e., the physiological basis for information transmission between neurons. Changes in the strength of synaptic connections are indeed thought to be the cellular basis of learning and memory. Importantly, astrocytes have been demonstrated to tightly regulate these processes via the release of several gliotransmitters linked to astrocytic calcium activity as well as astrocyte–neuron metabolic coupling. Therefore, astrocytes seem to be integrators of and actors upon learning- and memory-relevant information. In this review, we focus on the role of astrocytes in learning and memory processes. We delineate the recognized inputs and outputs of astrocytes and explore the influence of manipulating astrocytes on behaviour across diverse learning paradigms. We conclude that astrocytes influence learning and memory in various manners. Appropriate astrocytic Ca²⁺ dynamics are being increasingly identified as central contributors to memory formation and retrieval. In addition, astrocytes regulate brain rhythms essential for cognition, and astrocyte–neuron metabolic cooperation is required for memory consolidation. Full article

(This article belongs to the Special Issue Latest Review Papers in Molecular and Cellular Biology 2024)

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