Evidence map›Paper›PMID 41922997›Full record

ArticleBMC nephrology2026

The role of TOMM20 in Mediating TERT translocation to mitochondria and its impact on mitophagy in membranous nephropathy.

Limiao Yang, Hongle Yang, Mingming Zhang, Feifei Zhang, Xiaomei Liu, Zhiping Zhang, Jing Wang, Xiaolu Chen, Yuexuan Wang, Rui Zhang and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC nephrology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Limiao YangDepartment of Laboratory Medicine, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Hongle YangDepartment of Laboratory Medicine, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Mingming ZhangHebei Key Laboratory of Metabolic Diseases, Shijiazhuang, China.
Feifei ZhangSpecial Clinical Laboratory, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Xiaomei LiuSpecial Clinical Laboratory, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Zhiping ZhangSpecial Clinical Laboratory, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Jing WangSpecial Clinical Laboratory, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Xiaolu ChenSpecial Clinical Laboratory, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Yuexuan WangSpecial Clinical Laboratory, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Rui ZhangSpecial Clinical Laboratory, Second Hospital of Hebei Medical University, Shijiazhuang, China.
Weihao LiSpecial Clinical Laboratory, Second Hospital of Hebei Medical University, Shijiazhuang, China. 27500215@hebmu.edu.cn.

Funding

Government funded clinical medicine talent training Project ZF2023141Medical Science Research Project of Hebei 20230619
6 · The paper itself

Abstract

backgroundIn idiopathic membranous nephropathy (MN)—now a leading glomerular cause of end-stage kidney disease—mitochondrial quality control via mitophagy is increasingly recognized as a determinant of podocyte fate, yet the molecular switches governing this process remain undefined. We postulated that translocase of the outer mitochondrial membrane 20 (TOMM20), a gatekeeper of mitochondrial import, transcriptionally regulates telomerase reverse transcriptase (TERT) and thereby modulates podocyte mitophagy and disease progression.

methodsBioinformatics analysis was performed to identify common targets between mitophagy-related genes and differentially expressed genes in membranous nephropathy. An in vitro model of membranous nephropathy was established by treating human podocytes with Zymosan-Activated Serum (ZAS). Subsequently, cells were transfected to overexpress TOMM20 or knock down TERT. Cellular viability, apoptosis, and levels of inflammatory cytokines (IL-6, IL-1β) were assessed. Additionally, indicators related to mitophagy, including reactive oxygen species (ROS), mitochondrial membrane potential (MMP), LC3-II/I ratio, PTEN-induced putative kinase 1 (PINK1), Mitochondrial-associated Parkin protein (mito-Parkin), and p62 levels, were measured in each group. An in vivo model of membranous nephropathy was established by intravenously injecting rats with sheep anti-rat FX1A serum. The expression of TOMM20 was inhibited to investigate its effects on mitophagy and TERT mitochondrial translocation in membranous nephropathy.

resultBioinformatics analysis identified TOMM20 as a key target for intervening in the progression of membranous nephropathy via the mitochondrial pathway. In vitro, compared with human podocytes treated with heat-inactivated serum (HIS), ZAS intervention resulted in decreased cell viability, increased apoptosis, elevated levels of IL-6, IL-1β, and ROS, reduced MMP, decreased LC3-II/I ratio, PINK1, and mito-Parkin, and enhanced p62 expression. Overexpression of TOMM20 ameliorated ZAS-induced cell injury and enhanced mitophagy. Additionally, compared with the ZAS + Ctrl-siRNA group, knockdown of TERT exacerbated ZAS-induced cell injury and inhibited mitophagy. However, co-overexpression of TOMM20 promoted TERT mitochondrial translocation and mitigated the adverse effects of TERT-siRNA transfection in human podocytes. In vivo, upregulation of TOMM20 improved renal function in rats, promoted TERT mitochondrial translocation, and activated mitophagy.

conclusionTOMM20 activates mitophagy in membranous nephropathy by promoting the mitochondrial translocation and expression of TERT (The graphical abstract was shown in Fig. 1).

Indexed as

Glomerulonephritis, MembranousMitochondriaMitophagyPodocytesAnimalsApoptosisHumansMembrane Potential, MitochondrialMitochondrial Precursor Protein Import Complex ProteinsProtein TransportRatsMitochondrial Precursor Protein Import Complex ProteinsTOMM20 protein, humanTomm20 protein, ratMembranous nephropathyMitochondrial translocationMitophagyTelomerase reverse transcriptaseThe outer mitochondrial membrane 20

Identifiers

PMID41922997
PMCPMC13170007

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.