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lncRNA TUG1 and kidney diseases

BMC Nephrology volume 26, Article number: 139 (2025) Cite this article

Abstract

Long noncoding RNAs (lncRNAs) cover a large class of transcribed RNA molecules that are more than 200 nucleotides in length. An increasing number of studies have shown that lncRNAs control gene expression through different mechanisms and play important roles in a range of biological processes including growth, cell differentiation, proliferation, apoptosis, and invasion. TUG1 was originally discovered in a genomic screen of taurine-treated mouse retinal cells. Previous evidences pointed out that lncRNA TUG1 could inhibit apoptosis and the release of inflammatory factors, improve mitochondrial function, thereby protecting cells from damage, and showing a protective role of TUG1 in diseases. Given that TUG1 has multiple targets and can interfere with multiple steps in the oncogenic process, it has been proposed as a therapeutic target. In this review, we summarize the research progress of lncRNA TUG1 in kidney diseases in the past 8 years, and discuss its related molecular mechanisms.

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Kidney disease with mild inflammation, proteinuria, and function decline,or diagnosed with objective measures of kidney structure damage have been recognized as a major global health burden [1]. As a complex multi gene disease, the interaction and expression regulation of multiple genes often affect the occurrence and development of the kidney disease. Epigenetics has become one of the important mechanisms involved in the occurrence and development of kidney diseases by regulating gene transcription and translation [2].

lncRNAs cover a large class of transcribed RNA molecules that are more than 200 nucleotides in length [3,4,5,6]. In the past, non coding RNAs (ncRNAs) without the ability of coding protein were considered as non functional “junk” [7, 8]. However, increasing evidences have shown that lncRNAs control gene expression through different mechanisms and play important roles in a range of biological processes including growth, cell differentiation, proliferation, apoptosis, and invasion [9, 10]. lncRNAs have multiple modes of action, but are generally considered as important transcriptional regulators [3] (Fig. 1). In the cell nuclues, lncRNAs can regulate transcription factors (TF) as transcriptional co-activator or inhibitor. Enhancer RNAs are considered a subtype of lncRNA that are transcribed from the enhancer region and physically involved in looping the enhancer and promoter regions to regulate transcription. Some lncRNAs can act through DNA methylation, chromatin modification, histone modifications and RNA methylation, and to silence or enhance target gene expression. Other lncRNAs interfere with pre-mRNA splicing regulation [3, 11,12,13,14]. In the cytosol, lncRNAs can regulate mRNA expression by altering mRNA translation, stability, or by competing for microRNA binding [15,16,17]. Therefore, lncRNA is crucial in epigenetic regulation, gene transcription, gene translation, and mRNA processing, regulating various biological processes including in vivo balance, cell metabolism, proliferation, apoptosis, and differentiation [18,19,20].

Fig. 1
figure 1

lncRNAs regulate gene expressions at multiple levels.TF, transcription factor; SF, splicing factor; RBP, RNA binding protein

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Among all lncRNAs related to kidney disease, taurine upregulated gene 1 (TUG1) is a rising star. More and more evidences show that TUG1 plays an important role in many kidney diseases, such as acute kidney injury (AKI), chronic kidney disease (CKD), lupus nephritis (LN), diabetic kidney disease (DKD), renal interstitial fibrosis (RIF), glomerulonephritis, and renal cell carcinoma (RCC). The human lncRNA TUG1 gene (NCBI reference sequence NR_110492 transcript variant 1) is located on chromosome 22q12.2 and has 8 variant transcripts with a length range of 5.2–7.6 kb, while the mouse lncRNA TUG1 locus is located on chromosome 11 and has three variant transcripts (a, b, and c) with a length range of 4.1–6.7 kb [4]. TUG1 was originally discovered in a genomic screen of taurine-treated mouse retinal cells [21, 22]. The regulatory mechanisms of TUG1 gene expression involve its role as a molecular sponge for various microRNAs, which in turn modulate the expression of target genes or RBP affecting processes like cell proliferation, apoptosis, migration, cell cycle changes and inflammation in distinct diseases (relevant to endocrinology, metabolism, immunology, neurobiology) [23]. Previous evidences pointed out that lncRNA TUG1 could inhibit apoptosis and the release of inflammatory factors, improve mitochondrial function, thereby protecting cells from damage, showing a protective role of TUG1 in diseases [24]. Given that TUG1 has multiple targets and can interfere with multiple steps in the oncogenic process, it has been proposed as a therapeutic target [3]. In this review, we summarize the research progress of lncRNA TUG1 in kidney diseases in the past 9 years, and discuss its related molecular mechanism.

The biological function of TUG1 in kidney diseases

Kidney disease is an important public health problem. Although the function of lncRNA TUG1 remains unclear and somewhat controversial, It still has many significant research implications in kidney diseases (Fig. 2, Table 1).

Table 1. The regulatory machinery of TUG1 in kidney diseases
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Fig. 2
figure 2

The role of TUG1 in all kidney diseases. Abbreviation: ECM, extracellular matrix; ERS, endoplasmic reticulum stress; EMT, epithelial-mesenchymal transition

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AKI

AKI is defined by abnormalities of kidney function with an increase in serum creatinine (SCr) by 50% within 7 days or an increase in SCr by 0.3 mg/dl within 2 days or oliguria for ≥ 6 h. Models to mimic AKI in clinical practice usually include I/R, cisplatin and LPS. Growing evidences suggest that lncRNA TUG1 can regulate mRNA splicing, transcription, and expression of target genes by acting as microRNA (miRNA) sponges and protein scaffolds. Chen et al. found that lncRNA TUG1 alleviated I/R induced AKI via serving as a miR-494-3p sponge to disinhibit E-cadherin [18]. Chang et al. found that overexpressing lncRNA TUG1 attenuated the protective effect of total glucosides of paeony (TGP) on AKI induced by I/R via competing for miR-29 to improve phosphatase and tensin homolog (PTEN) expression [26]. Xu et al. found that knocking down lncRNA TUG1 by binding to miR-29 to silence PTEN can alleviate I/R-induced autophagy and improve AKI in rats [27]. Sheng et al. found that lncRNA TUG1 acts as an endogenous sponge of miR-144-3p, targeting nuclear respiratory factor 2 (Nrf2) to alleviate ischemia–reperfusion induced AKI [28]. Zhao et al. found that TUG1 alleviated LPS-induced podocyte injury by competing for miR-197 to disinhibit mitogen activated protein kinase1 (MAPK1) [29]. lncRNA TUG1 can also regulate mRNA expression by altering mRNA stability. Sun et al. found that lncRNA TUG1 attenuated I/R induced AKI by regulating the stability of Acyl-CoA synthetase long-chain family 4 (ACSL4) mRNA via interacting with RNA-binding protein serine/arginine-rich splicing factor 1 (SRSF1) [30]. Nrf2 is one of the key TF regulating cells against oxidative damage [31]. Wang et al. found that TUG1 can regulate Nrf2 as transcriptional co-activator to alleviate LPS induced AKI [32]. Amini N et aL. found that lncRNA TUG1 may be involved in process of gallic acid (GA) protecting the kidney against cisplatin-induced nephrotoxicity through antioxidant, anti-inflammatory, and anti-apoptosis properties, however the mechanism was unclear [33].

CKD

CKD is defined by abnormalities of kidney function and/or structure with implications for health and with a duration of > 3 months. Previous studies have shown that TUG1 participated in renal fibrosis and progression of CKD including RIF, DKD, LN, hypertensive nephropathy, glomerulonephritides.

RIF

RIF is characterized by excessive extracellular matrix deposition and involves EMT [34], and is a dynamically developing irreversible process leading to the destruction of tissue structure and loss of organ function [35, 36]. Animal models were considered at day 3, day 7 or day 14 after UUO and day 10 after UIRI in mice because a-SMA, TGF-β and EMT were increased [34, 37]. Zhang et al. found that silencing of the lncRNA TUG1 alleviated EMT via serving as a miR-141-3p sponge to inhibit β-catenin [34]. Another study established by Zhang et al. revealed that TUG1 inhibition upregulates miR-140-3p to ameliorate renal fibrosis in hyperuricemic rats by inhibiting cathepsin D (CtsD) [37]. Zhang et al. found that knockdown of lncRNA TUG1 by binding to miR-223-3p to aggravate klotho loss and worsen cellular senescence, whereas klotho-derived peptide 1 (KP1) can alleviate those fibrotic kidney disorders [38].

DKD

DKD begins with hyperglycemic stimuli, and is the most common and refractory microvascular complication of diabetes, and the main cause of end-stage renal disease (ESRD) worldwide. The main pathological characteristics of diabetes nephropathy are glomerulosclerosis, ECM deposition and tubulointerstitial fibrosis [39,40,41]. The concept of the renal tubular center of DKD emphasizes the key role of proximal tubule (PT) and tubulointerstitial part in the development of DKD [4, 42]. However, the glomerular theory, especially podocyte injury, has received particular attention in the process of DKD. The specific molecular characteristics and epigenetic modification in recent studies indicate that TUG1 plays a key role in the progress of DKD.

As miRNA sponges, Duan et al. found that lncRNA TUG1 acts as an endogenous sponge for miR-377, targeting peroxisome proliferator activated receptor gamma (PPAR γ) to alleviate mesangial cell proliferation and extracellular matrix accumulation in DN [43]. Wang et al. found that lncRNA TUG1 improves renal fibrosis in diabetes nephropathy by inhibiting miR-21 and promoting tissue inhibitor of metalloproteinase 3 (TIMP3) expression [44]. Wang et al. found that lncRNA TUG1 can inhibit the SIRT1 axis via endogenous competition of miR-29c-3p to regulate the injury of renal tubular epithelial cells mediated by endoplasmic reticulum stress in diabetes nephropathy models [39]. Wang et al. TUG1 directly sponged to miR-145-5p alleviating kidney injury in DN mice and decreasing the inflammatory response and fibrosis of high glucose-stimulated HK-2 cells via dual-specificity phosphatase 6 (DUSP6) pathway [45]. As enhancer, Li et al. and Long et al. found that decreasing of TUG1 are mainly located in glomerular podocytes of db/db mice and human diabetes kidney samples [3, 4]. The high glucose environment promotes the carbohydrate response element binding protein (ChREBP) inhibiting TUG1 transcription through the carbohydrate response elements (ChoRE) motif in the promoter region of TUG1 [46]. TUG1 acts as a bridge between the 400 kb upstream enhancer and promoter of Ppargc1a, interacting with the TUG1 binding site upstream of the Ppargc1a promoter region, triggering transcriptional upregulation of Ppargc1a mRNA, and then regulating mitochondrial function in podocytes by targeting the transcription factor PPARγ coactivator 1α (PGC-1α, encoded by Ppargc1a) [3, 4]. The decrease of PGC-1α level will lead to damage of mitochondrial function, which will lead to energy depletion, increase of reactive oxygen species (ROS) production, and eventually lead to the development of diabetes nephropathy [3, 4, 47]. As translational inhibitor, Lei et al. found that increasing of TUG1 by astragaloside IV (AS-IV) can alleviated inflammation and podocyte apoptosis via inhibiting TNFR-associated factor 5 (TRAF5) in DN rats [48]. Zang et al. found that overexpression of TUG1 could suppress the proliferation and ECM accumulation of mesangial cells via inhibiting the protein levels of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) in diabetes nephropathy [49]. lncRNA TUG1 can also act through DNA methylation. Zheng et al. revealed that TUG1 overexpression protected against STZ-induced renal lesions and renal fibrosis via inactivating MAPK1/extracellular signal-regulated kinase (ERK) signaling in DKD mouse in a methyltransferase 14 (METTL14)-dependent manner [50].

LN

LN is caused by autoimmune and inflammatory reactions which can activate complement cascades and proinflammatory pathways, injuring resident renal cells (including renal tubular cells, podocytes, mesangial cells and endothelial cells) [51]. Accumulating evidence has shown that lncRNA TUG1 plays a key role in inhibiting cell injury and inflammatory regulation. Cao et al. found that up-regulating lncRNA TUG1 by pyrrolidine dithiocarbamate (PDTC) can inhibite NF-κB on renal injury in SLE mice [24]. Liu et al. found that lncRNA TUG1 directly sponged to miR‐153‐3p alleviating LPS‐induced HRMC injury through regulation of Bcl‐2 in LN [52].

Other kidney diseases related to TUG1

For those patients with abnormalities in kidney function and/or structure who meet neither the definition of AKI nor CKD, the term acute kidney disease (AKD), has been introduced as an important construct to address this. AKD is defined by abnormalities of kidney function and/or structure with implications for health and with a duration of ≤ 3 months [25]. However, relevant study of TUG1 in AKD is barely established.

Heart and kidney are closely related in the clinical syndrome of heart failure (HF). It is now clear that renal dysfunction often occurs in all phenotypes of HF, and it is associated with higher mortality and morbidity [53]. Despite the multifactorial pathophysiology of CKD, renal artery sclerosis and chronic renal ischemia leading to CKD with worsened prognosis can be seen everywhere in clinical practice. Zhang et al. found that lncRNA TUG1 can promote angiotensin II(Ang II)–induced renal fibrosis via endogenous competition of miR-29b-3p by binding to mineralocorticoid receptor(MR) [54]. In the next year, Zhao et al. revealed that TUG1 was lowly expressed in CHF patients and was further downregulated in CHF patients complicated with progressive CKD [55].

Urinary non-coding RNAs are a promising non-invasive tool that can reflect kidney disease, assist in appropriate diagnosis, and guide therapeutic choices [10, 56,57,58]. Salazar Torres et al. found that lncRNA TUG1 is also present in urinary sediment, and its expression is significantly reduced in patients with biopsy-confirmed glomerulonephritides, especially those diagnosed with focal segmental glomerulosclerosis (FSGS) [11]. PGC-1 α and mitochondrial transcription factor A (TFAM) can also be detected in urine and are significantly correlated with TUG1 expression levels [10]. However, there was no significant correlation between the expression level of TUG1 and glomerular filtration rate (GFR), proteinuria, or albuminuria. Further studies are required to evaluate urinary TUG1 as a potential biomarker of glomerulonephritides in early stage other than ESRD, and to determine its association with kidney dysfunction and patient prognosis.

RCC is one of the top ten deadly malignant tumors in the world. Accumulating evidences showed that TUG1 play a crucial role in the progression of various cancers [59]. In earlier years, Wang et al.and Zhang et al. both found that the relative level of TUG1 was significantly higher in ccRCC tissues compared to the adjacent non-tumor tissues [60, 61]. In recent years, Liu et al. found that TUG1 can positively control yes-associated protein (YAP) expression and promote cell proliferation and migration in RCC by inhibiting miR-9 [62]. Li et al. found that knocking down TUG1 can inhibit the formation of RCC, including the proliferation, invasion, metastasis, and EMT process of ACHN cells, by suppressing vascular endothelial growth factor (VEGF) through endogenous competition of miR-299-3p [59].

Discussion and prospect

LncRNAs are ncRNA sequences, with cell or tissue specificity, poor conservation, and are expressed at low levels [63]. It plays an important role in multiple cellular processes [64]. TUG1, as a novel lncRNA, is predominantly located in the nucleus, and has been shown to be abnormally expressed in various types of kidney diseases, and its dysregulation is closely related to disease progression [65]. Current research are mainly focused on the abnormal expression of TUG1 in biopsies or cells, which could be used as potential biomarkers for the diagnosis, progression, and prognosis of kidney diseases and serve as therapeutic implications (Table 2). Interestingly, the results and conclusions seem inconsistent in AKI and CKD. Fortunately, the role of TUG1 in the study of DKD, LN, CKD with CHF and focal segmental glomerulonephritis is affirmative and protective despite of the differences of animal species and cell lines. However, the role of TUG1 in the studies of hypertensive nephropathy and RCC seems harmful. Nevertheless, it seems that TUG1 is closely related to podocyte injury, apoptosis, autophagy, regulation of inflammatory factors, mitochondrial bioenergetics, ECM accumulation, ERS, EMT, cell proliferation, invasion and migration (Fig. 1).

In AKI, despite of animal strains and cell lines used in the experiments, 75% of the published literature identify TUG1 of renal protective. The inconsistency of the effects of TUG1 on autophagy, cell apoptosis, and inflammatory factors mainly depends on the degree of damages to cells and mouse kidneys, these may be due to the differences in animal species, ischemia or reperfusion time, or distinct disease states. In CKD caused by renal fibrosis, the inconsistency of the effects of TUG1 mainly depends on animal species, the concentration and intervention time of TGF-β1, some may lack cell counting kit-8 assay. Also independently bred animal will undergo genetic drift over time, which may affect phenotypic differences and the consistency of experimental outcomes [66]. Moreover, as compared with mRNA, lncRNA has a wide range of variation and a shorter half-life [67], so it’s widely believed that one lncRNA can interact with multiple miRNAs and produce multiple transcripts, which may have opposite effects. Predicting and experimentally verifying lncRNA-miRNA interactions involves a combination of high-throughput experimental techniques like cross-linking and immunoprecipitation (CLIP) [68]; sophisticated computational models, including deep learning [69], network analysis [70,71,72,73], graph convolution [73], and matrix factorization [74, 75]; and experimental techniques for cellular location of events or interactions, including subcellular fractionation assay, RNA fuorescence in situ hybridization (FISH) assay, RNA Immunoprecipitation (RIP) PCR, luciferase assays and RNA pull-down assay. Most of the cited papers in this review varify a mechanism for lncRNA-miRNA interactions in the above-mentioned methods, but few only describe vague associations using overexpression and knockdown experiments or database prediction, leaving the strength of the evidence they present weak (Table 1). Furthermore, as TUG1 exists in both the nucleus and cytoplasm, and different miRNA and RBP targets of TUG1 may yield different conclusions, highlighting cellular location of events and stoichiometry of lncRNA and miRNA including cell lysate pull-down assays, total internal reflection fluorescence (TIRF)-based single-vesicle imaging assays and Argonaute (Ago)-based FISH can offer high specificity, sensitivity, and spatial resolution [76, 77]. Unfortunately, there are only 6 cited papers in this review provide comprehensive explanations (Table1). Additionally, different mouse and human cell lines may affect TUG1 expression and the significance of the cited works, for immortalization of cell lines can influence observed phenotypes by affecting differentiation potential, and maintaining or altering specific cellular functions and markers (Table 3). Thus, more resarch is needed to confirm the role of TUG1 in kidney diseases and may help address the etiology of diseases.

Table 2. Diagnostic and therapeutic implications of TUG1
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In summary, the regulatory network of TUG1 varies greatly in most biological processes. However, TUG1 seems to primarily mediate these processes by regulating transcription factors to affect target gene expression or sponging to miRNAs to inhibit target gene expression, while the upstream regulatory mechanisms of lncRNA TUG1 in kidney diseases are scarcely reported. With increasing research investment in lncRNAs, especially TUG1, the study of the TUG1 signaling pathway in kidney diseases may open up new ideas for many new therapeutic methods in the future, and TUG1 is expected to achieve clinical applications eventually.

Table 3. Different mouse and human cell lines may affect TUG1 expression and the significance of the cited works
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Data availability

No datasets were generated or analysed during the current study.

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Acknowledgements

We would like to thank Qiuling Fan(Department of Nephrology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine) for her help with the ideas and article revision.

Funding

This study was supported by Chinese Nature Science Foundation (No.82070754) of founder Qiuling Fan.

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  1. Department of Nephrology, Shenyang Seventh People’s Hospital, Shenyang, 110003, Liaoning, China

    Tong Chen & Jian Lu

  2. Department of Nephrology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200940, China

    Qiuling Fan

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Tong Chen conducted the literature search, collected, analysed and interpreted the data and drafted the first manuscript. Qiuling Fan and Jian Lu revised the manuscript for intellectual content. All authors have read and approved the final version of the manuscript.

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Chen, T., Lu, J. & Fan, Q. lncRNA TUG1 and kidney diseases. BMC Nephrol 26, 139 (2025). https://doiorg.publicaciones.saludcastillayleon.es/10.1186/s12882-025-04047-w

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