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Advances in Molecular Research of Kidney Diseases
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Advances in Molecular Research of Kidney Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: closed (20 March 2026) | Viewed by 3183

Special Issue Editor

Dr. Andrea Angioi

E-Mail Website
Guest Editor
Nephrology, Dialysis and Transplantation, ARNAS “Brotzu”, Cagliari, Italy
Interests: renal pathology; immune-mediated diseases; nephrology; onconephrology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, "Advances in Molecular Research of Kidney Disease", aims to showcase the latest breakthroughs in understanding the molecular mechanisms underlying kidney diseases. We invite high-quality research that includes biomolecular experiments, focusing on novel insights into the pathophysiology, diagnosis, and treatment of kidney disorders. Areas of interest include molecular genetics, biomarkers, cellular signaling pathways, and innovative therapeutic approaches such as bioartificial kidneys, SGLT2 inhibitors, and targeted gene therapies. Clinical studies that incorporate molecular or biomolecular experiments are particularly welcome. By highlighting these advancements, we aim to advance our understanding of kidney disease and contribute to the development of more effective interventions, ultimately improving patient outcomes.

Dr. Andrea Angioi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

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Keywords

  • molecular genetics
  • kidney disease
  • biomarkers
  • cellular signaling
  • target therapeutics
  • innovative treatments

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Published Papers (4 papers)

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Research

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21 pages, 6507 KB  
Article
High-Dose Voclosporin Protects Against Acute Kidney Injury via Regnase-2-Mediated NGAL MRNA Decay
by Kazuhiro Hasegawa, Yusuke Sakamaki, Masanori Tamaki, Sumiyo Yamaguchi, Shinji Miyakami, Chihiro Okinari, Miho Tada, Makoto Otsuka, Masanori Minato and Shu Wakino
Int. J. Mol. Sci. 2026, 27(7), 3150; https://doi.org/10.3390/ijms27073150 - 30 Mar 2026
Viewed by 293
Abstract
Acute kidney injury (AKI) is a major complication of lupus nephritis and kidney transplantation, inevitably causing ischemia–reperfusion (I/R) injury. We previously confirmed that high-dose voclosporin induces drug nephropathy through aberrant peroxisome accumulation. The latter induces increased renal indole-3-aceticT acid (IAA) production due to [...] Read more.
Acute kidney injury (AKI) is a major complication of lupus nephritis and kidney transplantation, inevitably causing ischemia–reperfusion (I/R) injury. We previously confirmed that high-dose voclosporin induces drug nephropathy through aberrant peroxisome accumulation. The latter induces increased renal indole-3-aceticT acid (IAA) production due to the decreased expression of the IAA-degrading enzyme indolethylamine N-methyltransferase (INMT). Conversely, INMT overexpression prevents this nephropathy, suggesting that high-dose voclosporin could enable a novel therapeutic approach. This prompted us to test whether INMT overexpression with high-dose voclosporin could avert nephrotoxicity and protect against I/R injury. Inmt-overexpressing mice treated with high-dose voclosporin exhibited absence of peroxisomal abnormalities and resistance to I/R injury. RNA sequencing revealed the downregulation of tubular injury markers NGAL (Lcn2) and KIM-1 (Havcr1) concurrent with significant cytokine suppression. Mechanistic analysis revealed the robust induction of Regnase-2, an mRNA decay factor, which directly targeted stem–loop structures within the 3′ untranslated region of Lcn2 and Havcr1, thereby promoting their degradation in proximal tubular cells. Importantly, Regnase-2 knockdown mice showed Lcn2 upregulation, mitochondrial dysfunction, and peroxisomal abnormalities culminating in AKI, underscoring its renal protective effects. High-dose voclosporin under Inmt overexpression promoted Regnase-2-mediated mRNA decay to suppress tubular injury. This protective effect extended beyond I/R to rhabdomyolysis- and lipopolysaccharide-induced AKI to prevent nephropathy. Our findings demonstrate the potential transformative therapeutic approach of administering high-dose voclosporin to promote the prophylactic effect of Regnase-2 augmentation against AKI in both native and transplanted human kidneys. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Kidney Diseases)
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16 pages, 10332 KB  
Article
Estradiol and Raloxifene Protect Ovariectomized Mice from Acute Kidney Injury via G Protein-Coupled Estrogen Receptor-Mediated Nuclear Factor Erythroid 2-Related Factor 2/Heme Oxygenase-1 Activation
by Yichuan Wang, Yanbo Song, Jingyu Dai, Xinxin Zhang, Lina Zhao, Yihua Mao and Maochao Ding
Int. J. Mol. Sci. 2026, 27(7), 3070; https://doi.org/10.3390/ijms27073070 - 27 Mar 2026
Viewed by 253
Abstract
Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury. Estradiol (E2) and the selective estrogen receptor modulator raloxifene (RAL) reduce organ dysfunction, potentially via heme oxygenase-1 (HO-1)–mediated antioxidant and anti-inflammatory effects. This study examined whether E2 and RAL protect against [...] Read more.
Renal ischemia–reperfusion injury (IRI) is a major cause of acute kidney injury. Estradiol (E2) and the selective estrogen receptor modulator raloxifene (RAL) reduce organ dysfunction, potentially via heme oxygenase-1 (HO-1)–mediated antioxidant and anti-inflammatory effects. This study examined whether E2 and RAL protect against IRI through G protein-coupled estrogen receptor (GPER)–dependent activation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/HO-1 pathway in ovariectomized (OVX) mice; OVX IRI mice were pretreated for four weeks with E2, RAL, RAL + ML385 (Nrf2 inhibitor), or RAL + G15 (GPER antagonist). Renal histology, inflammatory and oxidative markers, and nuclear Nrf2 levels were assessed; OVX IRI increased interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and malondialdehyde (MDA) and decreased superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH); nuclear Nrf2 was low in sham and OVX IRI groups. E2 and RAL improved renal function and histology, reduced inflammation and oxidative stress, restored GPER expression, increased nuclear Nrf2, and upregulated HO-1 and NAD(P)H:quinone oxidoreductase 1 (NQO1). Co-treatment with ML385 or G15 reversed RAL’s benefits, reduced nuclear Nrf2, and worsened injury; E2 and RAL exert renoprotective effects against OVX-related renal IRI in a manner consistent with GPER-dependent Nrf2 nuclear translocation, which suggests involvement of the downstream antioxidant gene activation pathway. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Kidney Diseases)
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19 pages, 1573 KB  
Article
Short-Term: Cellular Metabolism and Gene Expression During the Onset of Diabetic Kidney Disease: A Diabetes Mellitus Experimental Model
by Jéssica Encinas, Glaucia Veiga, Joyce Raimundo, Matheus Perez, Giuliana Petri, Renan Cavalheiro, Pedro Reis, Laura Maifrino, Beatriz Alves and Fernando Fonseca
Int. J. Mol. Sci. 2025, 26(19), 9676; https://doi.org/10.3390/ijms26199676 - 4 Oct 2025
Viewed by 1036
Abstract
Diabetes is a chronic disease with a rising global prevalence. Research focuses on understanding its metabolic implications and early signaling of disease onset and complications, particularly the interconnected effects on the kidneys and brain. The objective of this study was to evaluate the [...] Read more.
Diabetes is a chronic disease with a rising global prevalence. Research focuses on understanding its metabolic implications and early signaling of disease onset and complications, particularly the interconnected effects on the kidneys and brain. The objective of this study was to evaluate the expression profile in the genes Mct1, Mct4, Cd147, Hif-1α and Vegf for different biological matrices in rats induced to diabetes in the determined periods of 7, 21, 30 and 40 days. Methods: Wistar rats (160–180g, n = 68), divided into sham and diabetic groups, were evaluated according to tissue samples from the brain and kidney, using classical biochemical analyses and assessing temporal intergroup differential gene expression by qPCR. Additionally, immunohistochemical analysis was performed on kidney samples to evaluate collagen deposition. In the renal tissues, we observed a decrease in the expression of Hif-1α (21 vs. 30 days) and Vegf (21 vs. 40 days), accompanied by an increase in collagen deposition. In the brain, alterations were observed in all evaluated genes when comparing the early group (7 days) to the later groups (30 and 40 days). We observed that the evaluated genes, as well as the collagen deposition analyzed by immunohistochemistry, are related to metabolic changes that, over time, contribute to the worsening of diabetes and the progression of secondary diseases directly and/or indirectly involving the studied tissues. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Kidney Diseases)
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Other

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7 pages, 19063 KB  
Case Report
Steroid-Resistant Focal Segmental Glomerulosclerosis with Alport-like Glomerular Basement Membrane Lesions Due to a MYO1E Mutation: A Pediatric Case Report
by Andrea Angioi, Doloretta Piras, Nicola Lepori, Paola Bianco, Matteo Floris, Gianfranca Cabiddu, Antonella Barreca and Antonello Pani
Int. J. Mol. Sci. 2026, 27(6), 2838; https://doi.org/10.3390/ijms27062838 - 20 Mar 2026
Viewed by 343
Abstract
Steroid-resistant nephrotic syndrome (SRNS) in childhood frequently reflects monogenic podocytopathies in which immunosuppression is ineffective. Biallelic variants in MYO1E, encoding the class I myosin Myo1E, cause a distinctive form of focal segmental glomerulosclerosis (FSGS) often accompanied by “Alport-like” multilamination of the glomerular [...] Read more.
Steroid-resistant nephrotic syndrome (SRNS) in childhood frequently reflects monogenic podocytopathies in which immunosuppression is ineffective. Biallelic variants in MYO1E, encoding the class I myosin Myo1E, cause a distinctive form of focal segmental glomerulosclerosis (FSGS) often accompanied by “Alport-like” multilamination of the glomerular basement membrane (GBM). Early recognition has therapeutic and prognostic implications. A previously healthy 4-year-old boy presented with generalized edema and nephrotic-range proteinuria. Glucocorticoids induced no remission; sequential calcineurin inhibition (cyclosporine, then tacrolimus) and a single dose of ofatumumab yielded only transient, partial reductions in proteinuria. A first biopsy elsewhere showed FSGS with nonspecific IgM/C3 trapping; electron microscopy (EM) was not performed. At age 10, repeat biopsy with EM revealed ~30% segmental foot-process effacement, focal GBM thickening (to 1740 nm), irregular lamina densa multilamination, and lamellar duplications without immune-complex deposits—features highly suggestive of hereditary GBM disease. Targeted sequencing identified compound-heterozygous MYO1E variants segregating in trans: a canonical splice-donor change (c.2785+1G>A) and a frameshift (c.3094_3097del; p.Thr1032Profs*73). Each parent was an unaffected heterozygous carrier; the sibling was negative. Supportive therapy with ramipril was continued. At last follow-up (January 2025), renal function was normal (serum creatinine 0.5 mg/dL; creatinine clearance 122 mL/min) with stable sub-nephrotic proteinuria (0.52 g/day; 16 mg/m2 per hour) and normotension. This case broadens clinicopathologic recognition of MYO1E-associated nephropathy and highlights the teaching point that Alport-like GBM changes are not pathognomonic for type IV collagen disorders but may signal defects in podocyte cytoskeletal anchoring. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Kidney Diseases)
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