Utero-placental calcium and magnesium ion channels: A systematic review of obstetric implications of their alterations.

Authors

Gaudence Ndinganire, Aime Patrick Niyomugabo, Daniel Udofia Owu, Makinde Vincent Olubiyi, David Chibuike Ikwuka, Alphonse Niyodusenga, Mayowa Jeremiah Adeniyi, Muluken Walle, Onyinye Cynthia Okeke, Abdul-Rahuf Aderemi Feyitimi, Ejike Daniel Eze, Akaninyene Ubong Ime, Elemi John Ani, Abdulazeez Jimoh, Abdullahi Hussein Umar, Diresebachew Wondimu Haile, Abdullateef Isiaka Alagbonsi, Olufunke Onaadepo

Published in

Channels (Austin, Tex.). Volume 20. Issue 1. Pages 2724674. Epub Aug 26, 2026.

Abstract

Despite the established roles of calcium (Ca²⁺) and magnesium (Mg²⁺) in placental function and uterine contractility, limited information exists on how dysregulation of major ion channels contributes to poor pregnancy outcomes. We synthesized data on the consequences of Ca²⁺ and Mg²⁺ channelopathies in uterine and placental functions. Using PubMed, Wiley Online, AJOL, and Web of Science databases for article search, a systematic review of forty-nine papers published between 2000 and March 2026 was carried out and reported in accordance with the PRISMA 2020 guideline. Based on the PICO framework, eligible studies involving human, animal, and in vitro designs were chosen and subjected to narrative analysis. L-type and T-type voltage-gated Ca²⁺ channels, together with transient receptor potential channels, emerged as principal mediators of placental Ca²⁺ transport and myometrial contractility. Mechanosensitive Piezo1 channels mediate stretch-activated Ca²⁺ influx, while store-operated Ca²⁺ entry pathways involving STIM1-Orai1 sustain intracellular Ca²⁺ homeostasis. Potassium-Ca²⁺ coupling channels modulated membrane hyperpolarization and anti-labor effects, and intracellular regulators such as PMCA and RYR1 fine-tuned Ca²⁺ homeostasis. The Mg²⁺ transporters are essential for preserving Mg²⁺ homeostasis and regulating Ca²⁺-dependent excitability. Dysregulation of these ion channel systems was consistently linked to abnormal uterine contractility, preterm birth, preeclampsia, fetal growth restriction, and adverse pregnancy outcomes. Both Ca²⁺ and Mg²⁺ ion channelopathies represent both a potential therapeutic target and a mechanistic factor underlying key obstetric complications.

PMID:
42644398
Bibliographic data and abstract were imported from PubMed on 26 Aug 2026.

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