TOMM70

Last update 08 May 2025

Basic Info

Synonyms

KIAA0719, Mitochondrial import receptor subunit TOM70, Mitochondrial precursor proteins import receptor

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Introduction

Acts as a receptor of the preprotein translocase complex of the outer mitochondrial membrane (TOM complex) (PubMed:12526792). Recognizes and mediates the translocation of mitochondrial preproteins from the cytosol into the mitochondria in a chaperone dependent manner (PubMed:12526792, PubMed:35025629). Mediates TBK1 and IRF3 activation induced by MAVS in response to Sendai virus infection and promotes host antiviral responses during virus infection (PubMed:20628368, PubMed:25609812, PubMed:32728199). Upon Sendai virus infection, recruits HSP90AA1:IRF3:BAX in mitochondrion and the complex induces apoptosis (PubMed:25609812).

100 Clinical Results associated with TOMM70

100 Translational Medicine associated with TOMM70

0 Patents (Medical) associated with TOMM70

256

Literatures (Medical) associated with TOMM70

01 May 2025·Journal of Trauma and Acute Care Surgery

Cell-free mitochondria are detected in high concentrations in the plasma of orthopedic trauma patients

Article

Author: Meakes, Simone ; Balogh, Zsolt J ; Briggs, Gabrielle D ; King, Kate L

BACKGROUNDTrauma and surgery can derange inflammatory and hemostasis responses, potentially leading to multiple organ failure. Mitochondrial damage-associated molecular patterns are known to be part of the pathomechanism, but their exact origin remains uncertain. Recently, intact mitochondria were detected in healthy individuals' peripheral blood, which suggested a potential role in inflammation.METHODSIn this case-control study, we quantitated cell-free mitochondria in the blood of healthy subjects (n = 4) and trauma patients (n = 25) and assessed their relationship with patient demographics, injury and shock severity, markers of tissue injury, inflammation, and blood transfusions. Blood samples were collected before and after major orthopedic trauma surgery, and cell-free mitochondria were quantified using flow cytometry, targeting the outer mitochondrial membrane protein, TOMM70. Mitotracker Deep Red staining was used to assess mitochondrial membrane potential.RESULTSTrauma patients had significantly more cell-free mitochondria in their plasma compared with healthy controls, with highest counts immediately after surgery. The number of cell-free mitochondria decreased by day 5 postoperatively. Trauma patients exhibited a higher proportion of active cell-free mitochondria compared with healthy controls, especially immediately after surgery, and this proportion correlated with tissue injury markers. Associations were also found with acute thrombocytopenia, Denver multiple organ failure score, and transfusion of fresh frozen plasma and cryoprecipitate.CONCLUSIONOur findings indicate that the mere high number of cell-free mitochondria in the circulation of trauma patients is not necessarily pro-inflammatory, but their active status is associated with more severe secondary tissue injury. The natural history of cell-free mitochondria in trauma needs to be characterized, including their potential cause-effect relationship with major postinjury complications.LEVEL OF EVIDENCEPrognostic and Epidemiological; Level III.

01 May 2025·Veterinary Microbiology

The depletion of TFAM and p-β-catenin(S552) in mitochondria in response to BoAHV-1 productive infection leads to decreased mitochondrial biogenesis

Article

Author: Lin, Jiayu ; Ding, Xiuyan ; Fiorito, Filomena ; Fu, Xiaotian ; Li, Xuan ; Li, Shitao ; Zhu, Liqian

Varicellovirus bovinealpha (BoAHV) types 1(BoAHV-1) is one of the most significant viruses affecting cattle, causing substantial economic losses in the global cattle industry. Virus productive infection in cell cultures leads to mitochondrial dysfunction, resulting in the overproduction of reactive oxygen species (ROS), which act as inflammatory mediators and exert cytotoxic effects. But the underlying mechanisms remain poorly understood. Mitochondrial transcription factor A (TFAM) is a critical transcriptional activator of the mitochondrial DNA and plays a vital role in mitochondrial biogenesis. In this study, we report that virus acute infection in calves (at 4 days post-infection) increases TFAM protein expression and its accumulation in the peri-nuclear region in a subset of trigeminal ganglia (TG) neurons. Similarly, virus productive infection at later stages in MDBK cells also leads to increased TFAM protein expression and its accumulation in the nucleus. Using TFAM-specific siRNAs, we revealed that TFAM plays a significant role in BoAHV-1 productive infection. Consistent with decreased mitochondrial biogenesis, TFAM protein accumulation in mitochondria was significantly reduced following viral infection, which is corroborated by the reduced accumulation of TOM70 and Tim44 proteins in mitochondria. These proteins are key components of the mitochondrial membrane transport system that facilitates the translocation of TFAM into mitochondria. Interestingly, we found that a subset of β-catenin resides in mitochondria, and viral infection decreases the accumulation of transcriptionally active β-catenin, p-β-catenin(S552), in mitochondria. This may contribute to decreased mitochondrial biogenesis, as the β-catenin-specific inhibitor iCRT14 reduces the protein expression of Cytb, a key regulator of mitochondrial biosynthesis. Collectively, we suggest that the depletion of both TFAM and p-β-catenin(S552) in mitochondria may contribute to the mitochondrial dysfunction induced by BoAHV-1 productive infection.

01 Apr 2025·Atherosclerosis

Simvastatin ameliorates senescence-induced mitochondrial dysfunction in vascular smooth muscle cells

Article

Author: Battaglia, C ; Rossi, C ; Ruscica, M ; Venturin, M ; Corsini, A ; D'Alonzo, C ; Bellosta, S ; Macchi, C

BACKGROUND AND AIMSSenescence and mitochondrial dysfunction are two major indicators of aging. Mitochondria are potential drivers of aging phenotypes and dysfunctional mitochondria are associated with several age-related diseases. There is evidence that senescence induces changes in mitochondrial structure, dynamics, and function. Moreover, senescent vascular smooth muscle cells (VSMCs) are present in atherosclerotic plaques and contribute to their instability. The anti-atherosclerotic effects of simvastatin are well known, but recently other benefits, such as promoting mitochondrial quality and senostatic effects, have been hypothesized. We aimed to analyze simvastatin's senostatic effects in senescent VSMCs.METHODSWe established and characterized mitochondrial dysfunction in doxorubicin-induced senescent VSMCs (doxorubicin) or VSMCs serially passaged to induce replicative senescence (old).RESULTSWe observed in both senescent models few typical senescence markers such as altered cell morphology, cell cycle inhibitors, laminB1, an accumulation of dysfunctional mitochondria characterized by reduced mitochondrial membrane potential (MMP) and respiration, accumulation of reactive oxygen species (ROS), and an altered mitochondria morphology. Down-regulation of TFAM and TOM70 expression was observed only in old cells suggesting a reduction of mitochondrial biogenesis. Next, we investigated whether simvastatin could ameliorate age-associated phenotypes in senescent VSMCs. Simvastatin 0.1 μM reduces the senescence-associated secretory phenotype (SASP) and ROS production and improves mitochondrial respiration in doxorubicin and old VSMCs. Interestingly, the effects of simvastatin on mitochondrial respiration and SASP were replicated by using a siRNA for the hydroxy-methyl-glutaryl-coenzyme A (HMG-CoA) reductase, and abolished by adding mevalonic acid, suggesting that these effects are mediated through the inhibition of HMG-CoA reductase.CONCLUSIONSOur results suggest that simvastatin controls SASP and exerts potentially beneficial therapeutic effects by ameliorating senescence-induced mitochondrial dysfunction in senescent VSMCs.

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TOMM70

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