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YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE226787 | GEO | 2026/01/01

REPOSITORIES: GEO

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YTHDF1 mitigates acute kidney injury via safeguarding m<sup>6</sup>A-methylated mRNAs in stress granules of renal tubules.

Project description:Acute kidney injury (AKI) presents a daunting challenge with limited therapeutic options. To explore the contribution of N6-methyladenosine (m6A) in AKI development, we have investigated m6A-modified mRNAs within renal tubular cells subjected to injuries induced by diverse stressors. Notably, while the overall level of m6A-modified RNA remains unaltered in renal tubular cells facing stress, a distinct phenomenon emerges-mRNAs bearing m6A methylation exhibit a pronounced tendency to accumulate within stress granules (SGs), structures induced in response to these challenges. Cumulation of m6A-modified mRNA in SGs is orchestrated by YTHDF1, a m6A 'reader' closely associated with SGs. Strikingly, AKI patients and various mouse AKI models showcase elevated levels of renal tubular YTHDF1. Depleting YTHDF1 within renal tubular cells leads to a marked reduction in m6A-modified mRNA accumulation within SGs, accompanied by an escalation in cell apoptosis under stress challenges. The significance of YTHDF1's protective role is further underscored by findings in AKI mouse models triggered by cisplatin or renal ischemia-reperfusion treatments. In particular, renal tubular-specific YTHDF1 knockout mice exhibit heightened AKI severity when contrasted with their wild-type counterparts. Mechanistic insights reveal that YTHDF1 fulfills a crucial function by safeguarding m6A-modified mRNAs that favor cell survival-exemplified by SHPK1-within SGs amid stress-challenged renal tubular cells. Our findings collectively shed light on the pivotal role of YTHDF1 in shielding renal tubules against AKI, through its adeptness in recruiting and preserving m6A-modified mRNAs within stress-induced SGs.

| S-EPMC10587769 | biostudies-literature

YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [MeRIP]

Project description:The pathogenesis of acute kidney injury (AKI), a serious complication with no effective therapy available, is complex and multifactorial. Here we show that renal tubular m6A reader YTHDF1 mitigates AKI through selectively recruiting m6A-modified mRNAs, many of which are essential for cell proliferation and survival, into stress granules (SGs) and safeguarding these methylated mRNAs in SGs until stress relief. This study provides YTHDF1, as well as its associated m6A mRNAs and SGs, as novel therapeutic targets for AKI treatment.

2026-01-01 | GSE226784 | GEO

YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [RNA-Seq]

2026-01-01 | GSE226786 | GEO

YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [RIP-Seq]

2026-01-01 | GSE226785 | GEO

YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules

Project description:YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules

| PRJNA941795 | ENA

YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [MeRIP]

Project description:YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [MeRIP]

| PRJNA942051 | ENA

YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [RNA-Seq]

Project description:YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [RNA-Seq]

| PRJNA942049 | ENA

YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [RIP-Seq]

Project description:YTHDF1 mitigates acute kidney injury via safeguarding m6A-methylated mRNAs in stress granules of renal tubules [RIP-Seq]

| PRJNA942050 | ENA

Yeast m6A Methylated mRNAs Are Enriched on Translating Ribosomes during Meiosis, and under Rapamycin Treatment.

Project description:Interest in mRNA methylation has exploded in recent years. The sudden interest in a 40 year old discovery was due in part to the finding of FTO's (Fat Mass Obesity) N6-methyl-adenosine (m6A) deaminase activity, thus suggesting a link between obesity-associated diseases and the presence of m6A in mRNA. Another catalyst of the sudden rise in mRNA methylation research was the release of mRNA methylomes for human, mouse and Saccharomyces cerevisiae. However, the molecular function, or functions of this mRNA 'epimark' remain to be discovered. There is supportive evidence that m6A could be a mark for mRNA degradation due to its binding to YTH domain proteins, and consequently being chaperoned to P bodies. Nonetheless, only a subpopulation of the methylome was found binding to YTHDF2 in HeLa cells.The model organism Saccharomyces cerevisiae, has only one YTH domain protein (Pho92, Mrb1), which targets PHO4 transcripts for degradation under phosphate starvation. However, mRNA methylation is only found under meiosis inducing conditions, and PHO4 transcripts are apparently non-methylated. In this paper we set out to investigate if m6A could function alternatively to being a degradation mark in S. cerevisiae; we also sought to test whether it can be induced under non-standard sporulation conditions. We find a positive association between the presence of m6A and message translatability. We also find m6A induction following prolonged rapamycin treatment.

| S-EPMC4505848 | biostudies-literature

SARS-CoV-2 Causes Acute Kidney Injury by Directly Infecting Renal Tubules.

Project description:Acute kidney injury (AKI) is one of the most prevalent complications among hospitalized coronavirus disease 2019 (COVID-19) patients. Here, we aim to investigate the causes, risk factors, and outcomes of AKI in COVID-19 patients. We found that angiotensin-converting enzyme II (ACE2) and transmembrane protease serine 2 (TMPRSS2) were mainly expressed by different cell types in the human kidney. However, in autopsy kidney samples, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) nucleoprotein was detected in ACE2+ or TMPRSS2+ renal tubular cells, whereas the RNAscope® Assay targeting the SARS-CoV-2 Spike gene was positive mainly in the distal tubular cells and seldom in the proximal tubular cells. In addition, the TMPRSS2 and kidney injury marker protein levels were significantly higher in the SARS-CoV-2-infected renal distal tubular cells, indicating that SARS-CoV-2-mediated AKI mainly occurred in the renal distal tubular cells. Subsequently, a cohort analysis of 722 patients with COVID-19 demonstrated that AKI was significantly related to more serious disease stages and poor prognosis of COVID-19 patients. The progressive increase of blood urea nitrogen (BUN) level during the course of COVID-19 suggests that the patient's condition is aggravated. These results will greatly increase the current understanding of SARS-CoV-2 infection.

| S-EPMC8201778 | biostudies-literature

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