BNIP3

Last update 08 May 2025

Basic Info

Synonyms

BCL2 interacting protein 3, BCL2/adenovirus E1B 19 kDa protein-interacting protein 3, BNIP3

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Introduction

Apoptosis-inducing protein that can overcome BCL2 suppression. May play a role in repartitioning calcium between the two major intracellular calcium stores in association with BCL2. Involved in mitochondrial quality control via its interaction with SPATA18/MIEAP: in response to mitochondrial damage, participates in mitochondrial protein catabolic process (also named MALM) leading to the degradation of damaged proteins inside mitochondria. The physical interaction of SPATA18/MIEAP, BNIP3 and BNIP3L/NIX at the mitochondrial outer membrane regulates the opening of a pore in the mitochondrial double membrane in order to mediate the translocation of lysosomal proteins from the cytoplasm to the mitochondrial matrix. Plays an important role in the calprotectin (S100A8/A9)-induced cell death pathway.

100 Clinical Results associated with BNIP3

100 Translational Medicine associated with BNIP3

0 Patents (Medical) associated with BNIP3

1,782

Literatures (Medical) associated with BNIP3

01 Dec 2025·Molecular Biology Reports

Inhibiting HSP90 changes the expression pattern of PINK1 and BNIP3 and induces oxidative stress in colon cancer cells

Article

Author: Yousef, Tuqa ; Alzu'bi, Ayman ; Ai-Jariri, Heba F ; Abu-El-Rub, Ejlal ; Alomari, Amal ; Aldamen, Ala A ; Khaswaneh, Ramada R ; Almazari, Rawan ; Almahasneh, Fatimah A ; Kasasbeh, Amani ; Al-Zoubi, Raed M

AbstractBackgroundCancer cells can modulate the expression of many proteins that are essential for supporting their uncontrolled proliferation. Heat shock protein 90 (HSP90) is ubiquitously expressed in most cell types and participates in controlling many survival pathways. Cancer cells utilize HSP90 in order to prolong their survival, thus they tend to overexpress it. Based on its importance for cancer cells, we aim to investigate the molecular mechanisms that link HSP90 inhibition in colon cancer cells with oxidative stress and mitochondrial stress—related regulators.Materials and methodsWe used RKO colon cancer cells, blocking HSP90 with the inhibitor AT13387 and HSP90 siRNA. Cell proliferation and apoptosis were measured via CCK8 ELISA and Fluorescent Apoptosis Assays. Western blotting and immunocytochemistry assessed oxidative and mitochondrial stress markers BNIP3, PINK1, GP91/NOX2, and IRE1α in treated cells.ResultsOur findings reveal that inhibiting HSP90 with AT13387 reduces RKO cell viability by suppressing proliferation and enhancing Annexin-V expression, indicative of increased apoptosis. This rise in apoptosis is associated with PINK1 downregulation and BNIP3 upregulation, markers of mitochondrial dysfunction and oxidative stress, respectively. Additionally, AT13387 treatment elevated the protein level of GP91, a marker of oxidative stress, and IRE1α, a marker of ER stress. Similarly, genetic knockdown of HSP90 in RKO cells produced comparable effects, including reduced cell survival and a decreased PINK1/BNIP3 ratio.ConclusionTargeting HSP90 in colon cancer cells disrupts their survival by decreasing PINK1 and increasing BNIP3, which activates oxidative and endoplasmic reticulum stress, ultimately triggering apoptosis.

01 Aug 2025·Biomaterials

Manganese dioxide coupled metal-organic framework as mitophagy regulator alleviates periodontitis through SIRT1-FOXO3-BNIP3 signaling axis

Article

Author: Li, Ruomei ; Zhu, Zhiyu ; Huang, Kai ; Fang, Bing ; Li, Yixin ; Zhu, Cheng ; Xia, Lunguo ; Jin, Yu ; Yang, Shengbing ; Li, Tiancheng

Periodontitis is a prevalent chronic inflammatory disease characterized by alveolar bone resorption. Its progression is closely linked to oxidative stress where reactive oxygen species (ROS) generated by mitochondria exacerbate inflammation in positive feedback loops. Strategies for mitochondrial regulation hold potential for therapeutic advances. Metal-organic frameworks (MOFs) have shown promise as nanozymes for ROS scavenging. However, inability to directly regulate cellular processes to prevent further ROS production from damaged mitochondria during persistent inflammation makes MOFs insufficient in treating periodontitis. This study synthesizes MnO₂@UiO-66(Ce) by introducing MnO₂ within nanoscale mesoporous UiO-66 type MOFs. MnO₂ coupled with Ce clusters in MOF channels, forms a superoxide dismutase/catalase cascade catalytic system. More importantnly, manganese endows the MOFs with bioactive effects which enhances mitophagy, facilitating the removal of damaged mitochondria, thereby restoring long-term cellular homeostasis. The results demonstrate that this synergistic antioxidant solution MnO₂@UiO-66 restores mitochondrial homeostasis and osteogenic activity of periodontal ligament cells in vitro and alleviates inflammatory bone resorption in a ligature-induced periodontitis model in vivo. The SIRT1-FOXO3-BNIP3 signaling axis plays a key role in this process. This study may provide a design strategy that combines a highly efficient cascade catalytic system with long-term regulation of cellular homeostasis to combat oxidative stress in chronic inflammation.

01 Jun 2025·Fish & Shellfish Immunology

Hypoxia-induced mitochondrial dysfunction and mitophagy in the small yellow croaker (Larimichthys polyactis)

Article

Author: Wang, Li ; Liu, Feng ; Liu, Yang ; Zhu, Junquan ; Wang, Jingqian ; Lou, Bao ; Deng, Lu

Mitophagy serves as a pivotal mechanism for regulating the quantity and quality of mitochondria within cells, exerting significant influence on various processes such as cell differentiation, oxidative stress, inflammatory responses, and apoptosis. Currently, research on whether and how fish activate mitophagy under hypoxic stress conditions is still insufficient. In this study, to determine the mechanisms whereby marine fish adapt to hypoxic environments from the perspective of mitophagy, we used the small yellow croaker (Larimichthys polyactis) as the research subject and combined in vivo (liver) and in vitro (small yellow croaker fry [SYCF] cell line) hypoxic stress experiments. Fish exposed to hypoxic conditions were found to be characterized by liver tissue damage, and we detected significant elevations in the levels of hydrogen peroxide in liver tissues and reactive oxygen species (ROS) in SYCF cells, along with significant reductions in mitochondrial membrane potential. These findings thus indicate that hypoxic stress leads to tissue damage, excessive ROS production, and mitochondrial damage. In further experiments, we pre-treated SYCF cells with the antioxidant N-acetylcysteine, which was found to effectively reduce ROS levels and prevented the loss of mitochondrial membrane potential, thereby indicating that ROS play a crucial role in hypoxic stress-induced mitochondrial damage. Subsequently, to investigate whether hypoxic stress activates mitophagy to remove damaged mitochondria, we examined changes in the mRNA expression of mitophagy-related genes (bnip3, lc3b, bnip3l, beclin1, fundc1, and ulk1) in the liver and SYCF cells of L. polyactis exposed to hypoxic stress, and detected a significant upregulation of the mRNA expression of these genes. Furthermore, examination of liver ultrastructure and changes in the co-localization of mitochondria and lysosomes in SYCF cells revealed that hypoxic stress induces the formation of autophagosomes and autolysosomes in the liver, with an enhanced co-localization of mitochondria and lysosomes being observed after 6 h of hypoxia, which gradually increased with a prolongation of hypoxic exposure. We have, for the first time, exhibited the formation process of autophagosomes and the subsequent formation of autolysosomes in fish under hypoxic stress. These findings reveal the induction of mitophagy in L. polyactis in response to hypoxic stress, and indicate that these fish may initiate a mitophagic response to remove damaged mitochondria, reduce excessive ROS accumulation, and maintain cellular homeostasis. Our findings will not only lay a biological foundation for the breeding of hypoxia-tolerant strains of L. polyactis but also provide new insights into the mechanisms underlying the adaptation of marine fish to hypoxic environments.

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BNIP3

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