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Latest Review Papers in Molecular and Cellular Biology 2024
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Latest Review Papers in Molecular and Cellular Biology 2024

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 30 December 2024 | Viewed by 10982

Special Issue Editor

Prof. Dr. Stefano Papa

E-Mail Website
Guest Editor
Department of Biomolecular Sciences, University of Urbino Carlo Bo, 61029 Urbino, Italy
Interests: flow cytometry; apoptosis; exosomes; NK cells; melatonin
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to collect high quality review papers in all the fields of Molecular Biology. We encourage researchers from related fields to contribute review papers highlighting the latest developments in Molecular Biology, or to invite relevant experts and colleagues to do so. Full length comprehensive reviews will be preferred.

Prof. Dr. Stefano Papa
Guest Editor

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Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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Keywords

  • molecular biology
  • cell biology
  • signal transduction
  • macromolecules and complexes
  • gene expression
  • DNA structure, damage and repair
  • bioinformatics
  • imaging techniques

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Published Papers (7 papers)

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Review

13 pages, 408 KiB  
Review
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
Viewed by 677
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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25 pages, 3620 KiB  
Review
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
Viewed by 791
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  
Review
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
Viewed by 1201
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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22 pages, 2466 KiB  
Review
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
Viewed by 759
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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22 pages, 2268 KiB  
Review
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 1268
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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16 pages, 3079 KiB  
Review
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
Viewed by 1126
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  
Review
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 3 | Viewed by 4637
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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