International Journal of Molecular Sciences

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A Multifaceted Giant Protein Microtubule-Actin Cross-Linking Factor 1

by Chung-Ming Lin, Ru-Huei Fu and Hui-Jye Chen

Int. J. Mol. Sci. 2025, 26(7), 3204; https://doi.org/10.3390/ijms26073204 - 30 Mar 2025

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Microtubule-actin cross-linking factor 1 (MACF1), also known as actin cross-linking family protein 7 (ACF7), is a giant cytolinker protein with multiple conserved domains that can orchestrate cytoskeletal networks of actin and microtubules. MACF1 is involved in various biological processes, including cell polarity, cell–cell [...] Read more.

Microtubule-actin cross-linking factor 1 (MACF1), also known as actin cross-linking family protein 7 (ACF7), is a giant cytolinker protein with multiple conserved domains that can orchestrate cytoskeletal networks of actin and microtubules. MACF1 is involved in various biological processes, including cell polarity, cell–cell connection, cell proliferation, migration, vesicle transport, signal transduction, and neuronal development. In this review, we updated the physiological and pathological roles of MACF1, highlighting the components and signaling pathways involved. Novel evidence showed that MACF1 is involved in diverse human diseases, including multiple neuronal diseases, congenital myasthenic syndrome, premature ovarian insufficiency, spectraplakinopathy, osteoporosis, proliferative diabetic retinopathy, and various types of cancer. We also reviewed the physiological roles of MACF1, including its involvement in adhesome formation, bone formation, neuronal aging, and tooth development. In addition, MACF1 plays other roles, functioning as a biomarker for the prediction of infections in patients with burns and as a marker for genome selection breeding. These studies reinforce the idea that MACF1 is a bona fide versatile, multifaceted giant protein. Identifying additional MACF1 functions would finally help with the treatment of diseases caused by MACF1 defects. Full article

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

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19 pages, 1223 KiB

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Targeting Epigenetic Plasticity to Reduce Periodontitis-Related Inflammation in Diabetes: CBD, Metformin, and Other Natural Products as Potential Synergistic Candidates for Regulation? A Narrative Review

by Amelia Tero-Vescan, Mark Slevin, Amalia Pușcaș, Dragoș Sita and Ruxandra Ștefănescu

Int. J. Mol. Sci. 2025, 26(7), 2853; https://doi.org/10.3390/ijms26072853 - 21 Mar 2025

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Abstract

Periodontitis is unanimously accepted to be the sixth complication of diabetes mellitus (DM), while the inverse relationship of causality is still to be deciphered. Among the proposed mechanisms is gut dysbiosis, which is responsible for the systemic release of proinflammatory mediators. In this [...] Read more.

Periodontitis is unanimously accepted to be the sixth complication of diabetes mellitus (DM), while the inverse relationship of causality is still to be deciphered. Among the proposed mechanisms is gut dysbiosis, which is responsible for the systemic release of proinflammatory mediators. In this process, Gram-negative bacteria from the oral cavity enter the general circulation, leading to the emergence of bi-hormonal beta-pancreatic cells that lack the ability to secrete insulin. Additionally, epigenetic and adaptive mechanisms in affected cells may play a role in reducing inflammation. The release of reactive oxygen species, proinflammatory cytokines, and adipokines, such as interleukins, tumor necrosis factor alpha, leptin, prostaglandin E2, C-reactive protein, or matrix metalloproteinases, determine epigenetic changes, such as the methylation of DNA nucleotides or changes in the activity of histone acetylases/deacetylases. The management of periodontitis involves targeting inflammation, and its potential connection to epigenetic modulation observed in other chronic conditions may help to explain its role in preventing DM in affected patients. This review focuses on the key epigenetic changes in periodontitis that might contribute to DM development, and explores the mechanisms and novel multi-drug therapies that could help to prevent these effects. Full article

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

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18 pages, 751 KiB

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Influence of Klotho Protein Levels in Obesity and Sarcopenia: A Systematic Review

by Diana G. Ariadel-Cobo, Brisamar Estébanez, Elena González-Arnáiz, María Pilar García-Pérez, Marta Rivera-Viloria, Begoña Pintor de la Maza, David Emilio Barajas-Galindo, Diana García-Sastre, María D. Ballesteros-Pomar and María J. Cuevas

Int. J. Mol. Sci. 2025, 26(5), 1915; https://doi.org/10.3390/ijms26051915 - 23 Feb 2025

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Abstract

The Klotho gene is recognized for its anti-aging properties. Its downregulation leads to aging-like phenotypes, whereas overexpression can extend lifespan. Klotho protein exists in three forms: α-klotho, β-klotho and γ-klotho. The α-klotho has two isoforms: a membrane-bound form, primarily in the kidney and [...] Read more.

The Klotho gene is recognized for its anti-aging properties. Its downregulation leads to aging-like phenotypes, whereas overexpression can extend lifespan. Klotho protein exists in three forms: α-klotho, β-klotho and γ-klotho. The α-klotho has two isoforms: a membrane-bound form, primarily in the kidney and brain, and a secreted klotho protein present in blood, urine, and cerebrospinal fluid. Klotho functions as a co-receptor for fibroblast growth factor-23 (FGF23), regulating phosphate metabolism. The membrane-bound form controls various ion channels and receptors, while the secreted form regulates endocrine FGFs, including FGF19 and FGF21. The interaction between β-klotho and FGF21 in muscle is critical in the development of sarcopenic obesity. This systematic review, registered in PROSPERO and conducted following PRISMA guidelines, evaluates klotho levels in individuals with obesity or sarcopenic obesity. The study includes overweight, obese, and sarcopenic obese adults compared to those with a normal body mass index. After reviewing 713 articles, 20 studies were selected, including observational, cross-sectional, cohort studies, and clinical trials. Significant associations between klotho levels and obesity, metabolic syndrome (MS), and cardiovascular risk were observed. Exercise and dietary interventions positively influenced klotho levels, which were linked to improved muscle strength and slower decline. Klotho is a potential biomarker for obesity, MS, and sarcopenic obesity. Further research is needed to explore its mechanisms and therapeutic potential. Full article

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

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26 pages, 1908 KiB

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The MET Oncogene Network of Interacting Cell Surface Proteins

by Simona Gallo, Consolata Beatrice Folco and Tiziana Crepaldi

Int. J. Mol. Sci. 2024, 25(24), 13692; https://doi.org/10.3390/ijms252413692 - 21 Dec 2024

Viewed by 1362

Abstract

The MET oncogene, encoding the hepatocyte growth factor (HGF) receptor, plays a key role in tumorigenesis, invasion, and resistance to therapy, yet its full biological functions and activation mechanisms remain incompletely understood. A feature of MET is its extensive interaction network, encompassing the [...] Read more.

The MET oncogene, encoding the hepatocyte growth factor (HGF) receptor, plays a key role in tumorigenesis, invasion, and resistance to therapy, yet its full biological functions and activation mechanisms remain incompletely understood. A feature of MET is its extensive interaction network, encompassing the following: (i) receptor tyrosine kinases (RTKs); (ii) co-receptors (e.g., CDCP1, Neuropilin1); (iii) adhesion molecules (e.g., integrins, tetraspanins); (iv) proteases (e.g., ADAM10); and (v) other receptors (e.g., CD44, plexins, GPCRs, and NMDAR). These interactions dynamically modulate MET’s activation, signaling, intracellular trafficking, and degradation, enhancing its functional versatility and oncogenic potential. This review offers current knowledge on MET’s partnerships, focusing on their functional impact on signaling output, therapeutic resistance, and cellular behavior. Finally, we evaluate emerging combination therapies targeting MET and its interactors, highlighting their potential to overcome resistance and improve clinical outcomes. By exploring the complex interplay within the MET network of interacting cell surface proteins, this review provides insights into advancing anti-cancer strategies and understanding the broader implications of RTK crosstalk in oncology. Full article

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

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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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Abstract

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

Cited by 4 | Viewed by 2265

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 3 | Viewed by 4020

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

Viewed by 1972

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

Cited by 2 | Viewed by 2482

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

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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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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 3 | Viewed by 3310

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

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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 11 | Viewed by 3235

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 15 | Viewed by 10383

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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