Background/aim: Hepatocellular carcinoma is a substantial healthcare burden with high prevalence and poor prognosis. As such, efforts are continually made to uncover molecules relevant in cancer biology, that are exploitable as targets for therapy. The mitochondrion is the powerhouse of the cell and exhibits altered functionality in the malignant state, including aberrant regulation of apoptosis and cellular respiration. Augmenter of liver regeneration (ALR) is a multifunctional mitochondrial protein that demonstrates anti-oxidative and anti-apoptotic properties and plays a key role in liver regeneration.
Materials And Methods: The present study systematically reviews the available literature on the role of ALR in cancer.
Results: Systematic search of PubMed resulted in 12 studies discussing ALR in multiple types of cancer. More specifically, ALR appears to be up-regulated in malignant cells and tissues. Furthermore, treatment of cells with exogenous ALR shows an anti-apoptotic effect while silencing or inhibiting ALR decreases cell and tumor survival.
Conclusion: ALR clearly plays a role in cancer biology and demonstrates potential as a therapeutic target.
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Augmenter of Liver Regeneration Crotonylation Assists in Mitochondria-ER Contact to Alleviate Hepatic Steatosis.
Cell Mol Gastroenterol Hepatol
December 2024
Department of Cell Biology and the Municipal Key Laboratory for Liver Protection and Regulation of Regeneration, Capital Medical University, Beijing, People's Republic of China. Electronic address:
Background & Aims: Crotonylation (Kcr), a newly identified post-translation modification (PTM), has been confirmed to be involved in diverse biological processes and human diseases as well. Metabolic dysfunction-associated steatotic liver disease (MASLD) poses a serious threat to people's health. Augmenter of liver regeneration (ALR) is an important liver regulatory protein, and the insufficiency of ALR expression is reported to accelerate liver steatosis progression to liver fibrosis or even hepatic carcinoma (HCC).
View Article and Find Full Text PDFAugmenter of liver regeneration inhibits renal fibrosis during acute kidney injury to chronic kidney disease transition by regulating autophagic flux.
Arch Biochem Biophys
February 2025
Department of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China; Kuanren Laboratory of Translational Lipidology, Centre for Lipid Research, Second Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address:
Background: Augmenter of liver regeneration (ALR) is believed to protect against acute kidney injury (AKI). The objective of this study was to investigate the mechanisms of ALR in the transition from AKI to chronic kidney disease (CKD).
Methods: ALR Conditional Knockout (CKO) mice were bilateral renal artery clamped to induce AKI and CKD.
The impact of augmenter of liver regeneration in blunt liver trauma: An experimental model analysis.
Ulus Travma Acil Cerrahi Derg
July 2024
Department of Radiology, Etlik City Hospital, Ankara-Türkiye.
Background: Traumatic liver injury is an acute event that triggers liver repair. The augmenter of liver regeneration (ALR) has been identified as a growth factor involved in this process. This study evaluates the impact of ALR on isolated liver blunt trauma and examines its relationship with various time intervals.
View Article and Find Full Text PDFAugmenter of liver regeneration knockout aggravates tubular ferroptosis and macrophage activation by regulating carnitine palmitoyltransferase-1A-induced lipid metabolism in diabetic nephropathy.
Acta Physiol (Oxf)
July 2024
Department of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Aim: Ferroptosis is a novel type of programmed cell death that performs a critical function in diabetic nephropathy (DN). Augmenter of liver regeneration (ALR) exists in the inner membrane of mitochondria, and inhibits inflammation, apoptosis, and oxidative stress in acute kidney injury; however, its role in DN remains unexplored. Here, we aimed to identify the role of ALR in ferroptosis induction and macrophage activation in DN.
View Article and Find Full Text PDFLoss of nephric augmenter of liver regeneration facilitates acute kidney injury via ACSL4-mediated ferroptosis.
J Cell Mol Med
February 2024
Department of Nephrology, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Article Synopsis
- - Ferroptosis, linked to lipid buildup in cells, worsens acute kidney injury (AKI), but how this happens is not well understood.
- - In a study using mouse models and AKI patients, researchers found that reducing a protein called augmenter of liver regeneration (ALR) increased ferroptosis and damage to mitochondria while overexpressing ALR reduced these effects.
- - The study revealed that ALR interacts with another protein, ACSL4, to lower levels of harmful fatty acids and protect against ferroptosis, suggesting that enhancing ALR could be an effective approach for treating AKI.
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