AIFM1

Last update 08 May 2025

Basic Info

Synonyms

AIF, AIFM1, apoptosis inducing factor mitochondria associated 1

+ [7]

Introduction

Functions both as NADH oxidoreductase and as regulator of apoptosis (PubMed:17094969, PubMed:20362274, PubMed:23217327, PubMed:33168626). In response to apoptotic stimuli, it is released from the mitochondrion intermembrane space into the cytosol and to the nucleus, where it functions as a proapoptotic factor in a caspase-independent pathway (PubMed:20362274). Release into the cytoplasm is mediated upon binding to poly-ADP-ribose chains (By similarity). The soluble form (AIFsol) found in the nucleus induces 'parthanatos' i.e. caspase-independent fragmentation of chromosomal DNA (PubMed:20362274). Binds to DNA in a sequence-independent manner (PubMed:27178839). Interacts with EIF3G, and thereby inhibits the EIF3 machinery and protein synthesis, and activates caspase-7 to amplify apoptosis (PubMed:17094969). Plays a critical role in caspase-independent, pyknotic cell death in hydrogen peroxide-exposed cells (PubMed:19418225). In contrast, participates in normal mitochondrial metabolism. Plays an important role in the regulation of respiratory chain biogenesis by interacting with CHCHD4 and controlling CHCHD4 mitochondrial import (PubMed:26004228). Pro-apoptotic isoform. Has NADH oxidoreductase activity. Does not induce nuclear apoptosis.

100 Clinical Results associated with AIFM1

100 Translational Medicine associated with AIFM1

0 Patents (Medical) associated with AIFM1

2,309

Literatures (Medical) associated with AIFM1

01 Sep 2025·Comparative Biochemistry and Physiology Part D: Genomics and Proteomics

Biochemical indices, histological observations and transcriptome sequencing reveal the response mechanism of largemouth bass (Micropterus salmoides) to transport stress

Article

Author: Qiang, Jun ; Wang, Qing Chun ; Hua, Jixiang ; Duan, Xue Jun ; Tao, Yi Fan

In this study, transport conditions were simulated to investigate changes in intestinal tissue structure, oxidative stress, apoptosis and transcriptome levels during transport stress of largemouth bass (Micropterus salmoides). The results showed that the serum cortisol and lactic acid levels in largemouth bass significantly increased with increasing transport time, and the glucose content peaked after 8 h of transport. After 8 h and 12 h, the Reactive oxygen species, superoxide dismutase, malondialdehyde, and lipid peroxide contents in the intestine were significantly higher than those in the control group and the stressed group at 4 h. Additionally, more of the mucous membrane of intestinal tissue was exfoliated, resulting in edema, and the intestinal villi height and density significantly decreased. The differentially expressed genes were further analyzed after 0 h, 8 h, and 12 h of transport stress. There were significant differences in genes associated with the p53 signaling pathway (igfbp1a, ccnb1, cdk1, and igfbp6b) and apoptosis (bcl2l11, parp3, pik3r1, fadd, aifm1, and lmnb1). Combined with the increasing amount of apoptotic cells after stress, these results indicated that transport stress had a substantial effect on intestinal cell apoptosis. The intestinal antioxidant activity and tissue structure of the stressed groups recovered to the pre-stress level after 7 d of recovery from 8 h of transport; however, these parameters did not return to pre-stress levels after 7 d of recovery from 12 h of transport. This finding further demonstrated that long-term transport stress induced apoptosis and tissue damage in the largemouth bass intestine through p53 signaling.

01 Aug 2025·Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology

The crosstalk between autophagy and apoptosis mechanism of hemocytes in Chlamys farreri under B[a]P exposure in vitro

Article

Author: Tong, Ruixue ; Zhang, Ning ; Lei, Fengjun ; Liao, Qilong ; Li, Yaobing ; Pan, Luqing

The impact of polycyclic aromatic hydrocarbons (PAHs) on the immune function of marine animals has garnered significant attention. C. farrei is frequently exposed to pollutants and has only innate immunity. To delve more deeply into the immunotoxicity mechanism of PAHs in C. farrei, its hemocytes were cultured in vitro as they were the primary drivers of immune activities. The autophagy and apoptosis of hemocytes are essential components of the immune response. The exposure of pollutant, autophagy and apoptosis of immune cells are often disrupted, leading to immunodeficiency. In aquatic animals, the mechanism of autophagy and apoptosis in hemocytes remains unclear, and the crosstalk between the two needs to be further investigated. To evaluate the mechanism of autophagy and apoptosis of hemocytes in vitro, 0 μM, 1 μM, 2.5 μM or 5 μM Benzopyrene (B[a]p) was chosen. Experimental results demonstrated that B[a]P triggered autophagosome formation, but also caused significant damage to lysosomes, resulting in a compromised autophagic flux. B[a]P causes an increase in apoptosis levels in hemocytes of C. farreri by affecting the transcriptional level of AIF. To further explore the crosstalk mechanism between the two, activator and inhibitor of autophagy were used. After adding autophagy activator or inhibitor, the present results indicated that Lysosomal function determined the patency of autophagic flux. When massive autophagosomes accumulate, it leads to a much higher rate of apoptosis through caspase-dependent apoptotic pathway. Lysosomal damage further leads to apoptosis and inhibit autophagy. In the B[a]P-treated group, immunological parameters were markedly decreased due to autophagy and apoptosis of hemocytes. The immunotoxicity mechanism of B[a]P in C. farreri hemocytes was investigated in present study, which enriched the immunotoxicity network.

01 Jun 2025·Toxicology Reports

IONPs-induced neurotoxicity via cascade of neuro-oxidative stress, parthanatos-mediated cell death, neuro-inflammation and neurodegenerative changes: Ameliorating effect of rosemary methanolic extract

Article

Author: Khayal, Eman El-Sayed ; Ahmed, Mona Mostafa ; Abd-Almotaleb, Noha Ali ; Elsheikh, Arwa A

Iron oxide nanoparticles (IONPs) are widely used in various fields, particularly in medicine, where they can be directly injected for diagnostic and therapeutic purposes, although they may induce certain types of toxicity. Therefore, the present work aimed to estimate the potential protective role of the oral extract of rosemary (RO)against the toxic effects of injected IONPs on the brain tissues of adult male rats, and to explore the potential underlying mechanisms involved in reversing such toxicity. Thirty adult male albino rats were allocated into five groups: the control, the vehicle (intravenous saline injection once/week), the RO extract group (orally gavaged100mg/kg/day), IONPs (intravenously injected 30 mg/kg once/week), and the combined RO+IONPs (orally gavaged RO extract 1 hrh before intravenous injection of IONPs). IONPs induced neurotoxicity via triggering a cascade of neuro-oxidative stress, neuro-inflammation, and parthanatos-mediated neuronal cell death by increasing MDA, NO, TNF-α levels, PARP-1, AIF, and NF-κB mRNA expression alongside reducing GSH levels. These incidents contributed to neurodegenerative changes, reflected in increased mRNA expression of α-S, β-APP, and TDP-43. Additionally, IONPs induced structural degenerative changes and elevated iron levels in brain tissues reduced occludin expression, and disrupted the BBB. Furthermore, the concurrent oral RO extract alleviated these conditions and repaired BBB by increasing the occludin expression and ameliorating structural changes in brain tissues. Consequently, the current data provide evidence that RO supplementation during IONP administration holds promise to minimize potential health risks, which should be corroborated by translational studies.

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AIFM1

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