ArticleFrontiers in pharmacology2011
Recent advances in the pathogenesis and drug action in periodic paralyses and related channelopathies.
Article in Frontiers in pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Open-Label, Dose-Escalation, Phase 1 Study of Safety and Single and Multiple-Dose Pharmacokinetics of Dichlorphenamide in Healthy Volunteers.Clinical pharmacology in drug development · 2019Trial
- Quantitative Muscle MRI to Monitor Disease Progression in Hypokalemic Period Paralysis.Neurology. Genetics · 2024Article
- Hypokalemic periodic paralysis: a 3-year follow-up study.Journal of neurology · 2023Article
- CaInternational journal of molecular sciences · 2023Review
- IncreasedNeurology. Genetics · 2018Article
- A leaky voltage sensor domain of cardiac sodium channels causes arrhythmias associated with dilated cardiomyopathy.Scientific reports · 2018Article
- Pre-clinical symptoms of SBMA may not be androgen-dependent: implications from two SBMA mouse models.Human molecular genetics · 2018Article
- Review of the Diagnosis and Treatment of Periodic Paralysis.Muscle & nerve · 2018Review
- A New Cardiac Channelopathy: From Clinical Phenotypes to Molecular Mechanisms Associated With NaFrontiers in cardiovascular medicine · 2018Review
- Mechanisms Responsible for ω-Pore Currents in CaBiophysical journal · 2017Article
- Commentary: A BK (Slo1) channel journey from molecule to physiology.Frontiers in pharmacology · 2017Article
- Therapeutic Approaches to Genetic Ion Channelopathies and Perspectives in Drug Discovery.Frontiers in pharmacology · 2016Review
- Gating pore currents are defects in common with two Nav1.5 mutations in patients with mixed arrhythmias and dilated cardiomyopathy.The Journal of general physiology · 2015Article
- Mutations in the Voltage Sensors of Domains I and II of Nav1.5 that are Associated with Arrhythmias and Dilated Cardiomyopathy Generate Gating Pore Currents.Frontiers in pharmacology · 2015Article
- Protein kinase C theta (PKCθ) modulates the ClC-1 chloride channel activity and skeletal muscle phenotype: a biophysical and gene expression study in mouse models lacking the PKCθ.Pflugers Archiv : European journal of physiology · 2014Article
- The large-conductance calcium-activated potassium channel holds the key to the conundrum of familial hypokalemic periodic paralysis.Korean journal of pediatrics · 2014Article
- Article
- NaV1.4 mutations cause hypokalaemic periodic paralysis by disrupting IIIS4 movement during recovery.Brain : a journal of neurology · 2014Article
- Biophysics, pathophysiology, and pharmacology of ion channel gating pores.Frontiers in pharmacology · 2014Review
- Channelopathies.Korean journal of pediatrics · 2014Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The periodic paralysis (PP) are rare autosomal-dominant disorders associated to mutations in the skeletal muscle sodium, calcium, and potassium channel genes characterized by muscle fiber depolarization with un-excitability, episodes of weakness with variations in serum potassium concentrations. Recent advances in thyrotoxic PP and hypokalemic PP (hypoPP) confirm the involvement of the muscle potassium channels in the pathogenesis of the diseases and their role as target of action for drugs of therapeutic interest. The novelty in the gating pore currents theory help to explain the disease symptoms, and open the possibility to more specifically target the disease. It is now known that the fiber depolarization in the hypoPP is due to an unbalance between the novel identified depolarizing gating pore currents (I(gp)) carried by protons or Na(+) ions flowing through aberrant alternative pathways of the mutant subunits and repolarizing inwardly rectifying potassium channel (Kir) currents which also includes the ATP-sensitive subtype. Abnormal activation of the I(gp) or deficiency in the Kir channels predispose to fiber depolarization. One pharmacological strategy is based on blocking the I(gp) without affecting normal channel gating. It remains safe and effective the proposal of targeting the K(ATP), Kir channels, or BK channels by drugs capable to specifically open at nanomolar concentrations the skeletal muscle subtypes with less side effects.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.