Current topics in membranes最新文献

{"title":"Nerve electrophysiological alterations in experimental diabetic neuropathy.","authors":"Kerly Shamyra da Silva-Alves, Francisco Walber Ferreira-da-Silva, Bianca de Sousa Barbosa-Ferreira, Kylvia Rocha de Castro-E-Silva, Jeremias Martins-Gonçalves, Romário Pinheiro-Lustosa, Yuri Abreu Gomes-Vasconcelos, Maria Diana Moreira-Gomes, Andrelina Noronha Coelho-de-Souza, José Henrique Leal-Cardoso","doi":"10.1016/bs.ctm.2026.04.001","DOIUrl":"https://doi.org/10.1016/bs.ctm.2026.04.001","url":null,"abstract":"<p><p>Peripheral diabetic neuropathy (PDN) is a complication of diabetes mellitus that affects nerves and has great epidemiological and clinical relevance. It affects more than 2/3 of diabetic patients, compromising their quality of life and life expectancy. This chapter reviews the main electrophysiological alterations in excitability and conductibility observed in sciatic (somatic) and vagus (autonomic) nerves in experimental models of PDN, with emphasis on nerve extracellular recording. Initially, the clinical and pathophysiological aspects of PDN are outlined, followed by a brief review of experimental models of diabetes, particularly those induced by streptozotocin. The electrophysiological basis of compound action potential (CAP) generation is described, and key CAP parameters are discussed as indicators of functional nerve integrity. Experimental evidence demonstrates that diabetes induces consistent alterations in the sciatic nerve, characterized by reduced CAP amplitude and conduction velocity, increased duration of CAP waves, reflecting increased temporal dispersion of CAP components, and decreased nerve excitability. These changes worsen with disease duration and higher glycemic levels and may be detected even in pre-diabetic conditions. In contrast, the vagus nerve exhibits a more selective pattern of dysfunction. Recent experimental studies reveal that diabetes mellitus, at least at initial stages of disease evolution, preferentially affects myelinated vagal fibers, leading to reduced conduction velocity, increased component duration, and excitability, while unmyelinated fibers remain relatively preserved. Overall, the findings summarized in this chapter support the use of CAP recordings as a robust experimental approach for investigating the progression and mechanisms of PDN and for evaluating potential therapeutic interventions.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"98 ","pages":"1-24"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chemically induced cardiotoxicity: Role of voltage dependent ion channels.","authors":"Diego Jose Belato Orts, Aimée Obolari Durço, Michael Ramon de Lima Conceição, Jorge Lucas Teixeira-Fonseca, Julliane Vasconcelos Joviano-Santos, Danilo Roman-Campos","doi":"10.1016/bs.ctm.2026.02.001","DOIUrl":"10.1016/bs.ctm.2026.02.001","url":null,"abstract":"<p><p>Chemicals pervade human environments, with> 350,000 synthetic compounds driving unintentional exposures and pollution-linked deaths exceeding those from infectious diseases or violence. This review discusses the mechanisms of chemically induced cardiotoxicity (including pesticides, pollutants, heavy metals, and chemotherapeutics), emphasizing modulation of voltage-gated ion channels in cardiomyocytes, which disrupts action potential (AP) dynamics, excitation-contraction coupling (ECC), and predisposes to arrhythmogenesis. Key currents, sodium (I_Na), calcium (I_CaL, I_CaT), and potassium (I_to, I_Kr, I_K1), are differentially altered. Pyrethroid pesticides (e.g., deltamethrin) amplify late I_Na, prolong AP, and trigger afterdepolarizations. Organochlorines (e.g., aldrin) suppress peak I_Na; organophosphates, carbamates, and fungicides (e.g., tebuconazole) inhibit I_CaL, I_Na, and K+ currents, often via oxidative stress. Glyphosate-based herbicides impair I_CaL; rodenticides (e.g., phosphides) block K+ hERG channel, mimicking Brugada syndrome. Environmental pollutants lack direct ion-channel block properties evidence but provoke arrhythmias via inflammation/fibrosis (diesel exhaust), NO/redox inhibition (CO: I_Na, hERG, K_ir), current enhancement (SO₂: I_Na, I_to, I_CaL), or ROS-CaMKII activation (particulate matter). Heavy metals attenuates channels class-specifically: Pb²⁺ (I_CaL), Ni²⁺ (I_CaT), Cd²⁺ (I_Na, I_CaL), Hg²⁺ (I_to, I_CaL); Se/Zn modulate K⁺/Ca₂₊ currents in deficiency/excess. Chemotherapeutics exacerbate cardiovascular risk: anthracyclines (e.g., doxorubicin) boost I_CaL and RyR2 leak; platinums delay I_Na decay; TKIs (e.g., ibrutinib) broadly suppress currents kinase-dependently. Integrating in vitro/experimental molecular data, this review maps class-specific electrophysiological impacts in the heart, highlighting safety pharmacology's role in risk mitigation and informing therapeutic, regulatory, and public health strategies to safeguard cardiovascular resilience against pervasive chemical threats.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"97 ","pages":"19-58"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preface.","authors":"","doi":"10.1016/S1063-5823(26)00016-5","DOIUrl":"https://doi.org/10.1016/S1063-5823(26)00016-5","url":null,"abstract":"","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"97 ","pages":"xi"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834895","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thyroid hormone deficiency-induced cardiac ion channel dysfunction: Molecular mechanisms and arrhythmic implications.","authors":"Luiz Fernando Santos Matos, Emanuel Barbosa Dos Santos, Camila Souza Gama Rocha, João Víctor Santos Gomes, Natalia Rocha Medeiros Marques, Diego Santos Souza","doi":"10.1016/bs.ctm.2026.01.002","DOIUrl":"10.1016/bs.ctm.2026.01.002","url":null,"abstract":"<p><p>Thyroid hormones are essential regulators of cardiac excitability, contractility, and rhythm. Hypothyroidism induces profound electrophysiological remodeling through both genomic and non-genomic pathways, leading to altered expression and function of key ion channels, including HCN, Kv, and Ca²⁺-handling proteins. These changes result in reduced pacemaker activity, prolonged repolarization, and impaired excitation-contraction coupling, which collectively contribute to bradycardia, QT prolongation, and increased arrhythmogenic risk. Elevated thyroid-stimulating hormone (TSH) levels further exacerbate electrical instability through direct myocardial signaling. Experimental and clinical evidence indicates that many of these abnormalities could be reversible upon thyroid hormone replacement, emphasizing the importance of early diagnosis and multidisciplinary management. Understanding the molecular basis of thyroid-induced electrical remodeling provides insight into arrhythmogenesis and may guide therapeutic strategies to prevent cardiac complications in hypothyroidism.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"97 ","pages":"59-87"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834905","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiological insights into ion channel dysregulation and electrical remodeling in cardiac cells during Trypanosoma cruzi infection.","authors":"Ivan Lobo de Sousa Marques, Mario Henrique Veiga Meireles, Julliane Vasconcelos Joviano-Santos, Danilo Roman-Campos, Artur Santos-Miranda","doi":"10.1016/bs.ctm.2026.01.003","DOIUrl":"10.1016/bs.ctm.2026.01.003","url":null,"abstract":"<p><p>Chagas disease (CD), caused by Trypanosoma cruzi, affects 6-7 million people globally. Its most severe form, chagasic cardiomyopathy (CCM), develops in ∼30 % of infected individuals after a long latency and is highly lethal, with sudden cardiac death responsible for most fatalities. CCM is fundamentally an arrhythmogenic cardiomyopathy marked by early and profound electrical remodeling driven by ion channel dysfunction, often preceding structural damage. Its pathogenesis is complex, emerging from parasite-host interactions that disrupt immune signaling, microvascular function, contractility, autonomic balance, and cellular electrophysiology. In this context, ion channel dysfunction becomes central, shaped directly by these pathogenic mechanisms and indirectly by metabolic alterations and the inflammatory/infectious milieu. This chapter explores the known ion channel abnormalities in CCM and their relationship to the inflammatory environment, detailing the roles of ion handling, oxidative stress, and metabolic disturbances in electrical remodeling. Parasite ion channels are also discussed as potential therapeutic targets.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"97 ","pages":"89-117"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834886","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Possible therapeutic effects of essential oils on voltage dependent Na⁺ channels in experimental diabetic neuropathy.","authors":"Francisco Walber Ferreira-da-Silva, Romário Pinheiro-Lustosa, Francisca Edilziane Rodrigues-da-Silva, Jane Lane de Oliveira-Sandes, Jeremias Martins-Gonçalves, Yuri Abreu Gomes-Vasconcelos, Maria Diana Moreira-Gomes, Andrelina Noronha Coelho-de-Souza, José Henrique Leal-Cardoso, Kerly Shamyra da Silva-Alves","doi":"10.1016/bs.ctm.2026.04.002","DOIUrl":"https://doi.org/10.1016/bs.ctm.2026.04.002","url":null,"abstract":"<p><p>Diabetic neuropathy (DN) is the most frequent complication of diabetes mellitus (DM), characterized by derangements of somatic and autonomic nerves, predominantly the longest nerves. DN is clinically relevant because it may seriously damage the quality of life of the patient, may be life-threatening, and is of great epidemiological incidence. It causes severe pain, dysesthesia, and allodynia initially; with disease progression, it kills the nerve, leading to full anaesthesia, accidental feet, leg ulceration, diabetic foot, and amputation. Underlying these dysfunctional alterations, there are nerves and neurosomes electrophysiological alterations, which mechanism knowledge will likely disclose therapeutic targets offering opportunities for the development of new medicines. The electrophysiological derangements include alteration of excitability, of velocity of conduction, and of the inward Na⁺ current that causes the neuronal action potential. There is no specific treatment for DN. Investigation of the Laboratory of Electrophysiology (LEF) of Ceará State University, Ceará, Brazil, has discovered several DM-induced neural alterations. It has also discovered that the essential oil of the Croton zehntneri (a plant of the biome caatinga of Northeast of Brazil), and its major chemical constituent, anethole, is able to fully prevent some important electrophysiological neural alterations of experimental DN without hyperglycaemia correction. This prevention without restoration to euglycaemia suggests the usefulness of this essential oil and anethole as a medicine complementary to hypoglycaemic agents for the treatment of DN. These results, together with discoveries from other laboratories that are specifically related to the results of LEF investigation will be presented in this chapter.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"98 ","pages":"25-54"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Voltage gated ion channels and breast cancer.","authors":"Letícia Expedita Alves Dantas, Joana Menezes da Cunha Farias, Igor Guimarães Honorato, Daniel Alves de Souza, Bárbara Stephanie Santiago, Ana Maria Bernal Correa, Enilton Aparecido Camargo, Christopher Kushmerick, Andreia Laura Prates Rodrigues","doi":"10.1016/bs.ctm.2026.05.001","DOIUrl":"https://doi.org/10.1016/bs.ctm.2026.05.001","url":null,"abstract":"<p><p>Breast cancer is the leading form of cancer in women worldwide. Despite extensive research efforts to develop detection methods and treatment, mortality remains high. Biomarkers and therapeutic targets are needed. Tumoral cell express ion channels which may serve both functions. Expression of specific ion channels by neoplastic cells within tissues that normally do not express those channels, or expression of embryonic splice variants may be useful markers for early detection. Ion channels associated with metastatic potential or cell migration may also be useful therapeutic targets.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"98 ","pages":"55-87"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419527","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardioprotective effect of natural products on doxorubicin-induced cardiotoxicity and cardiac ischemia-reperfusion injury: A focus on ion channels modulation.","authors":"Lucas Andrade De Sá, Lorrane Nere De Lima, Douglas Costa Andrade, Jocsã Hémany Cândido-Santos, Bernardo Rocha Melo, Carlos Alberto Santana-Souza, Andreia Laura Prates Rodrigues, Sandra Lauton-Santos","doi":"10.1016/bs.ctm.2026.04.003","DOIUrl":"https://doi.org/10.1016/bs.ctm.2026.04.003","url":null,"abstract":"<p><p>This article reviews the cardioprotective effects of natural products against doxorubicin (DOX)-induced cardiotoxicity and ischemia-reperfusion (I/R) injury, focusing on the modulation of ion channels and oxidative stress. Both conditions share lethal pathophysiological pathways driven by the overproduction of reactive oxygen species (ROS) and intracellular calcium (Ca²⁺) overload, culminating in the opening of the mitochondrial permeability transition pore (mPTP) and cardiomyocyte apoptosis. Bioactive compounds-including polyphenols (such as quercetin and resveratrol), terpenes (such as geraniol and carvacrol), and alkaloids (such as berberine)-exert robust pleiotropic protection. These molecules directly modulate sarcolemmal and mitochondrial ion channels (such as Ca_v1.2, Na_v1.5, and mK_ATP), stabilize the action potential duration (APD), and activate intracellular survival cascades (Nrf2, SIRT1, AMPK). Although preclinical trials demonstrate high efficacy, the clinical translation of these findings still faces structural challenges, such as low bioavailability, the need for phytochemical standardization, and safety-related risks. The use of biotechnological delivery systems and the exploration of synergies with conventional therapies consolidate secondary metabolites as invaluable and highly promising adjuvant tools for the structural and electrophysiological protection of the myocardium.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"98 ","pages":"89-118"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preface.","authors":"","doi":"10.1016/S1063-5823(26)00030-X","DOIUrl":"https://doi.org/10.1016/S1063-5823(26)00030-X","url":null,"abstract":"","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"98 ","pages":"xi"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148419554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATP-sensitive potassium channels in neurons: Roles in and beyond metabolic control.","authors":"Ricardo Maurício Leão, Mariane Martins Migliaccio, Daniela Ferreira de Siqueira, Patrik Saul Zarpellon","doi":"10.1016/bs.ctm.2026.01.001","DOIUrl":"10.1016/bs.ctm.2026.01.001","url":null,"abstract":"<p><p>ATP-sensitive potassium (K_ATP) channels are part of the inwardly rectifying potassium (K_ir) channel family and are distinguished by their inhibition by intracellular ATP. Their role in pancreatic β-cells is well understood: increases in ATP production after glucose intake lead to K_ATP channel closure, causing membrane depolarization and insulin secretion. In the central nervous system, K_ATP channels are also abundant and are involved in glucose sensing and neuroprotection. However, their functions beyond these traditional roles are less certain. In this review, we examine the various actions of neuronal K_ATP channels in different brain regions, including those involved in metabolic regulation and others not directly linked to energy balance, highlighting emerging physiological functions of these channels beyond metabolic control.</p>","PeriodicalId":11029,"journal":{"name":"Current topics in membranes","volume":"97 ","pages":"1-18"},"PeriodicalIF":0.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}