{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T06:07:30Z","timestamp":1789106850295,"version":"build-2803163510"},"reference-count":71,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T00:00:00Z","timestamp":1789084800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Cell Dev. Biol."],"abstract":"<jats:p>\n                    Mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    homeostasis is a critical interface connecting ovarian cell signaling, energy metabolism, redox balance, and reproductive competence. Transient Ca\n                    <jats:sup>2+<\/jats:sup>\n                    uptake into the mitochondrial matrix activates Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -sensitive dehydrogenases, enhances reducing-equivalent generation, and supports oxidative phosphorylation. By contrast, sustained Ca\n                    <jats:sup>2+<\/jats:sup>\n                    accumulation promotes reactive oxygen species production, membrane-potential collapse, mitochondrial permeability transition, and cell death. The identification of the mitochondrial calcium uniporter together with its regulators MICU1, MICU2, and EMRE, has established a molecular framework for mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    influx. NCLX and its interacting protein TMEM65 contribute to Ca\n                    <jats:sup>2+<\/jats:sup>\n                    efflux and determine recovery after individual Ca\n                    <jats:sup>2+<\/jats:sup>\n                    transients. In ovarian cells and oocytes, endoplasmic reticulum (endoplasmic reticulum)-mitochondria contact sites, including the IP\n                    <jats:sub>3<\/jats:sub>\n                    R1-GRP75-VDAC1 axis, couple cytosolic Ca\n                    <jats:sup>2+<\/jats:sup>\n                    signals to mitochondrial metabolism. Evidence from mouse, porcine, avian, zebrafish,\n                    <jats:italic>Xenopus<\/jats:italic>\n                    , and sea-urchin models implicates mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    in follicular-cell survival, oocyte meiotic maturation, fertilization-associated Ca\n                    <jats:sup>2+<\/jats:sup>\n                    oscillations, the oocyte-to-embryo transition, and early embryonic development. Obesity, aging, cryopreservation, heavy metals, environmental chemicals, and oxidative stress can disturb this system. However, mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    dysregulation is not always readily separable from broader mitochondrial or ER dysfunction. Major limitations of the current literature include reliance on non-selective pharmacological agents, incomplete calibration of organelle-targeted indicators, insufficient temporal resolution, interspecies differences, and limited direct evidence from human oocytes. Future studies should integrate cell-type-specific genetic perturbation, quantitative multi-organelle Ca\n                    <jats:sup>2+<\/jats:sup>\n                    imaging, mitochondrial bioenergetics, and long-term developmental assessment. Mitochondrial Ca\n                    <jats:sup>2+<\/jats:sup>\n                    is a promising mechanistic node and candidate biomarker, but it is not yet a validated clinical target in reproductive medicine.\n                  <\/jats:p>","DOI":"10.3389\/fcell.2026.1963467","type":"journal-article","created":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T05:30:14Z","timestamp":1789104614000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Mitochondrial Ca2+ homeostasis in ovarian function and oocyte competence: from molecular transporters to early embryonic development"],"prefix":"10.3389","volume":"14","author":[{"given":"Xiaoqian","family":"Fu","sequence":"first","affiliation":[{"name":"The First Affiliated Hospital of Guangxi Medical University","place":["Nanning, Guangxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qianyi","family":"Huang","sequence":"additional","affiliation":[{"name":"The First Affiliated Hospital of Guangxi Medical University","place":["Nanning, Guangxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Huimei","family":"Wu","sequence":"additional","affiliation":[{"name":"The First Affiliated Hospital of Guangxi Medical University","place":["Nanning, Guangxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lidan","family":"Liu","sequence":"additional","affiliation":[{"name":"The First Affiliated Hospital of Guangxi Medical University","place":["Nanning, Guangxi, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,9,11]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"902","DOI":"10.1016\/j.tem.2024.03.002","article-title":"Mitochondrial morphology, distribution and activity during oocyte development","volume":"35","author":"Bahety","year":"2024","journal-title":"Trends Endocrinol. 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