https://journal3.um.ac.id/index.php/mipa <table width="100%" cellpadding="0" bgcolor="#ffffff"> <thead> <tr> <td colspan="4"> </td> </tr> <tr> <td width="17%">Title</td> <td width="3%">:</td> <td width="50%"><strong>Jurnal MIPA dan Pembelajarannya</strong></td> <td rowspan="10" align="right" bgcolor="#ffffff" width="40%"><a title="to learn more about our journal" href="http://journal3.um.ac.id/index.php/mipa"><img src="http://journal3.um.ac.id/public/site/images/budiarto/11c6cf6a9ef443e7d0b1707fae904dd6.png" alt="" width="150%" /></a></td> </tr> <tr> <td>Initials</td> <td>:</td> <td><strong>JMIPAP</strong></td> </tr> <tr> <td>Publications</td> <td>:</td> <td><strong>12 Issues every year</strong></td> </tr> <tr> <td>DOI</td> <td>:</td> <td><strong>prefix <a href="https://search.crossref.org/?q=jmipap&amp;from_ui=yes" target="_blank" rel="noopener">10.17977/um067</a> by </strong><strong>crossref</strong></td> </tr> <tr> <td>Acreditation</td> <td>:</td> <td> </td> </tr> <tr> <td>Print ISSN</td> <td>:</td> <td>-</td> </tr> <tr> <td>Online ISSN</td> <td>:</td> <td><strong><a href="https://portal.issn.org/resource/ISSN/2798-0634" target="_blank" rel="noopener">2798-0634</a></strong></td> </tr> <tr> <td>Editor-in-chief</td> <td>:</td> <td><strong>Nuril Munfaridah ,S.Pd, M.Pd, Ph.D</strong></td> </tr> <tr> <td>Publisher</td> <td>:</td> <td><strong>Universitas Negeri Malang</strong></td> </tr> <tr> <td>Email</td> <td>:</td> <td><strong>[email protected]</strong></td> </tr> <tr> <td>Journal Summary</td> <td>:</td> <td colspan="2"><br /> <p>Jurnal MIPA dan Pembelajarannya (JMIPAP) is a peer-reviewed scientific journal dedicated to the advancement of knowledge in mathematics, natural sciences, applied sciences, and science education. The journal serves as an academic platform for researchers, educators, scholars, and practitioners to disseminate original research findings, theoretical studies, reviews, and innovative scientific ideas that contribute to the development of science and education at national and international levels.</p> <p>JMIPAP encourages interdisciplinary perspectives and promotes scientific communication across diverse fields of mathematics and natural sciences. The journal welcomes contributions that explore both fundamental and applied aspects of science, as well as studies focusing on educational practices, curriculum development, learning innovation, instructional technology, and contemporary issues in science and mathematics education.</p> <p>The journal aims to support the integration of scientific research and educational advancement by providing high-quality publications that are relevant, impactful, and accessible to the wider academic community. JMIPAP is committed to maintaining academic integrity, rigorous peer-review standards, and ethical publication practices in order to ensure the quality and credibility of published articles.</p> <p>By fostering collaboration among researchers, educators, and professionals from various disciplines, JMIPAP aspires to become a reputable international forum for scientific discussion, innovation, and scholarly exchange in mathematics, natural sciences, applied sciences, and science education.</p> </td> </tr> </thead> </table> <p> </p> <p> </p> en-US [email protected] (Nuril Munfaridah ,S.Pd, M.Pd, Ph.D) [email protected] (Budiarto) Thu, 04 Jun 2026 00:18:07 +0000 OJS 3.3.0.5 http://blogs.law.harvard.edu/tech/rss 60 https://journal3.um.ac.id/index.php/mipa/article/view/8391 <p><strong>Background: </strong>Type 2 diabetes mellitus is a disease of progressively dysfunctional pancreatic β-cells, including β-cell apoptosis, where mitochondrial oxidative stress is a key pathogenic factor. Nevertheless, the molecular pathway which connects chronic hyperglycemia with mitochondrial Complex I dysfunction is not fully understood. <strong>Aim: </strong>The study examined the role of hyperglycemia-induced succinylation of the NDUFV2 subunit as an allosteric modulator of mitochondrial Complex I, increased reactive oxygen species (ROS) generation, and β-cell death. <strong>Methodology: </strong>A mechanistic study was planned with the use of INS-1 β-cells under normoglycemic (5.5 mmol/L) and hyperglycemic (25 mmol/L) conditions after 48 h of incubation, with osmotic controls, antioxidant treatment, SIRT5 overexpression, and site-directed mutagenesis of NDUFV2. Immunoprecipitation, immunoblotting and LC-MS/MS were used to assess NDUFV2 succinylation, while standard mitochondrial and cell-death assays were used to measure Complex I activity, oxygen consumption, ATP production, membrane potential, ROS generation and apoptosis. <strong>Results: </strong>Hyperglycemia elevated NDUFV2 succinylation 2.71-fold, mitochondrial ROS 2.31-fold, and caspase-3/7 activity 2.87-fold, and decreased Complex I activity to 58% and ATP to 24.8 nmol/mg protein. The K81R mutant restored Complex I activity to 88%, lowered ROS to 1.34-fold, and enhanced viability to 89%. <strong>Conclusion: </strong>NDUFV2 succinylation may be one of the mechanistic causes of Complex I impairment and ROS-induced β-cell apoptosis in type 2 diabetes.</p> Zainab Nasser Hussein Copyright (c) 2026 Zainab Nasser Hussein https://creativecommons.org/licenses/by-sa/4.0 https://journal3.um.ac.id/index.php/mipa/article/view/8391 Tue, 02 Jun 2026 00:00:00 +0000