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Molecular Mechanism of Diabetic Kidney Disease (2nd Edition)
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Molecular Mechanism of Diabetic Kidney Disease (2nd Edition)

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 November 2024) | Viewed by 13372

Special Issue Editor

Prof. Dr. Ligia Petrica

E-Mail Website
Guest Editor
Department of Nephrology, Centre for Molecular Research in Nephrology and Vascular Disease, "Victor Babes" University of Medicine and Pharmacy Timisoara, Timisoara, Romania
Interests: chronic kidney disease; diabetic kidney disease; epigenetics; proteomics; lipidomics; metabolomics; mitochondrial dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Diabetic kidney disease (DKD), as a major microvascular complication of both type 1 and type 2 diabetes mellitus (DM), accounts for over 40% of patients who reach end-stage renal disease and are referred to renal replacement therapies.

The tubulocentric concept with regard to DKD has emphasized the pivotal role of the proximal tubule and of the tubulointerstitial compartment in the development of DKD. The glomerular theory raises a similar interest, with a special focus on the contribution of podocyte injury in the course of DKD.

Chronic systemic inflammation and the role of inflammatory response in the development and progression of chronic kidney disease DKD have been highly recognized.

An inflammatory response which involves the innate immune system, as well as epigenetic mechanisms, plays an important role in the development of albuminuria in the course of type 2 DM. Particular molecular signatures and epigenetic profiles have emerged to support the complexity of DKD.

Mitochondrial dysfunction plays many specific roles in the pathogenesis of DKD. The importance of mitochondria in the pathogenesis of DKD resides in both the tubulocentric view and the mitochondria-centric view. Mitochondrial injury to glomerular endothelial cells and podocytes is also important for the development of DKD.

We are particularly taking interest in original papers and reviews that report the relevance of the molecular mechanisms involved in the pathogenesis of DKD.

Prof. Dr. Ligia Petrica
Guest Editor

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Keywords

  • genetics
  • epigenetics
  • inflammation
  • mitochondrial dysfunction
  • proteomics
  • lipidomics
  • metabolomics

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Published Papers (6 papers)

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Research

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15 pages, 4225 KiB  
Article
Sigma-1 Receptor as a Novel Therapeutic Target in Diabetic Kidney Disease
by Dora B. Balogh, Judit Hodrea, Adar Saeed, Marcell Cserhalmi, Alexandra Rozsahegyi, Tamas Lakat, Lilla Lenart, Attila J. Szabo, Laszlo J. Wagner and Andrea Fekete
Int. J. Mol. Sci. 2024, 25(24), 13327; https://doi.org/10.3390/ijms252413327 - 12 Dec 2024
Viewed by 1088
Abstract
Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease. Current treatments for DKD do not halt renal injury progression, highlighting an urgent need for therapies targeting key disease mechanisms. Our previous studies demonstrated that activating the Sigma-1 receptor (S1R) with [...] Read more.
Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease. Current treatments for DKD do not halt renal injury progression, highlighting an urgent need for therapies targeting key disease mechanisms. Our previous studies demonstrated that activating the Sigma-1 receptor (S1R) with fluvoxamine (FLU) protects against acute kidney injury by inhibiting inflammation and ameliorating the effect of hypoxia. Based on these, we hypothesized that FLU might exert a similar protective effect in DKD. Diabetes was induced in male Wistar rats using streptozotocin, followed by a seven-week FLU treatment. Metabolic and renal parameters were assessed along with a histological analysis of glomerular damage and fibrosis. The effects of FLU on inflammation, hypoxia, and fibrosis were tested in human proximal tubular cells and normal rat kidney fibroblasts. FLU improved renal function and reduced glomerular damage and tubulointerstitial fibrosis. It also mitigated inflammation by reducing TLR4, IL6, and NFKB1 expressions and moderated the cellular response to tubular hypoxia. Additionally, FLU suppressed TGF-β1-induced fibrotic processes and fibroblast transformation. These findings suggest that S1R activation can slow DKD progression and protect renal function by modulating critical inflammatory, hypoxic, and fibrotic pathways; therefore, it might serve as a promising novel drug target for preventing DKD. Full article
(This article belongs to the Special Issue Molecular Mechanism of Diabetic Kidney Disease (2nd Edition))
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7 pages, 234 KiB  
Communication
Serpin Family B Member 2 Polymorphisms in Patients with Diabetic Kidney Disease: An Association Study
by Maria Tziastoudi, Georgios Pissas, Spyridon Golfinopoulos, Georgios Filippidis, Christina Poulianiti, Evangelia E. Tsironi, Efthimios Dardiotis, Theodoros Eleftheriadis and Ioannis Stefanidis
Int. J. Mol. Sci. 2024, 25(20), 10906; https://doi.org/10.3390/ijms252010906 - 10 Oct 2024
Cited by 1 | Viewed by 967
Abstract
Diabetic kidney disease (DKD) is a serious microvascular complication of type 2 diabetes mellitus (T2DM). Despite the numerous genetic loci that have been associated with the disease in T2DM, the genetic architecture of DKD remains unclear until today. In contrast to SERPINE1, [...] Read more.
Diabetic kidney disease (DKD) is a serious microvascular complication of type 2 diabetes mellitus (T2DM). Despite the numerous genetic loci that have been associated with the disease in T2DM, the genetic architecture of DKD remains unclear until today. In contrast to SERPINE1, the contribution of SERPINB2 has not been examined in DKD. Therefore, we conducted the first genetic association study of SERPINB2 to elucidate its role in DKD. In total, the study involved 197 patients with DKD, 155 patients with T2DM without microvascular complications (diabetic kidney disease, diabetic retinopathy, and diabetic neuropathy), and 246 healthy controls. The generalized odds ratio (ORG) was calculated to estimate the risk on DKD development. The present association study regarding SERPINB2 SNPs (rs4941230, rs3819335, rs13381217, rs6140) did not reveal any significant association between SERPINB2 variants and DKD. Additional studies in other populations are necessary to further investigate the role of this gene in the progression of diabetes mellitus and development of DKD. Full article
(This article belongs to the Special Issue Molecular Mechanism of Diabetic Kidney Disease (2nd Edition))
19 pages, 5103 KiB  
Article
Mannan-Binding Lectin Is Associated with Inflammation and Kidney Damage in a Mouse Model of Type 2 Diabetes
by Gry H. Dørflinger, Charlotte B. Holt, Steffen Thiel, Jesper N. Bech, Jakob A. Østergaard and Mette Bjerre
Int. J. Mol. Sci. 2024, 25(13), 7204; https://doi.org/10.3390/ijms25137204 - 29 Jun 2024
Cited by 1 | Viewed by 1580
Abstract
Autoreactivity of the complement system may escalate the development of diabetic nephropathy. We used the BTBR OB mouse model of type 2 diabetes to investigate the role of the complement factor mannan-binding lectin (MBL) in diabetic nephropathy. Female BTBR OB mice (n [...] Read more.
Autoreactivity of the complement system may escalate the development of diabetic nephropathy. We used the BTBR OB mouse model of type 2 diabetes to investigate the role of the complement factor mannan-binding lectin (MBL) in diabetic nephropathy. Female BTBR OB mice (n = 30) and BTBR non-diabetic WT mice (n = 30) were included. Plasma samples (weeks 12 and 21) and urine samples (week 19) were analyzed for MBL, C3, C3-fragments, SAA3, and markers for renal function. Renal tissue sections were analyzed for fibrosis, inflammation, and complement deposition. The renal cortex was analyzed for gene expression (complement, inflammation, and fibrosis), and isolated glomerular cells were investigated for MBL protein. Human vascular endothelial cells cultured under normo- and hyperglycemic conditions were analyzed by flow cytometry. We found that the OB mice had elevated plasma and urine concentrations of MBL-C (p < 0.0001 and p < 0.001, respectively) and higher plasma C3 levels (p < 0.001) compared to WT mice. Renal cryosections from OB mice showed increased MBL-C and C4 deposition in the glomeruli and increased macrophage infiltration (p = 0.002). Isolated glomeruli revealed significantly higher MBL protein levels (p < 0.001) compared to the OB and WT mice, and no renal MBL expression was detected. We report that chronic inflammation plays an important role in the development of DN through the binding of MBL to hyperglycemia-exposed renal cells. Full article
(This article belongs to the Special Issue Molecular Mechanism of Diabetic Kidney Disease (2nd Edition))
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Review

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20 pages, 1238 KiB  
Review
New Perspectives in Studying Type 1 Diabetes Susceptibility Biomarkers
by Yongsoo Park, Kyung Soo Ko and Byoung Doo Rhee
Int. J. Mol. Sci. 2025, 26(7), 3249; https://doi.org/10.3390/ijms26073249 - 31 Mar 2025
Viewed by 402
Abstract
Type 1 diabetes (T1D) is generally viewed as an etiologic subtype of diabetes caused by the autoimmune destruction of the insulin-secreting β-cells. It has been known that autoreactive T cells unfortunately destroy healthy β-cells. However, there has been a notion of etiologic heterogeneity [...] Read more.
Type 1 diabetes (T1D) is generally viewed as an etiologic subtype of diabetes caused by the autoimmune destruction of the insulin-secreting β-cells. It has been known that autoreactive T cells unfortunately destroy healthy β-cells. However, there has been a notion of etiologic heterogeneity around the world implicating a varying incidence of a non-autoimmune subgroup of T1D related to insulin deficiency associated with decreased β cell mass, in which the β-cell is the key contributor to the disease. Beta cell dysfunction, reduced mass, and apoptosis may lead to insufficient insulin secretion and ultimately to the development of T1D. Interestingly, Korean as well as other ethnic genetic results have also suggested that genes related with insulin deficiency, let alone those of immune regulation, were associated with the risk of T1D in the young. Genes related with insulin secretion may influence the phenotype of diabetes differentially and different genes may be working on different steps of T1D development. Although we admit the consensus that islet autoimmunity is an essential component in the pathogenesis of T1D, however, dysfunction might occur not only in the immune system but also in the β-cells, the defect of which may induce further dysfunction of the immune system. These arguments stem from the fact that the β-cell might be the trigger of an autoimmune response. This emergent view has many parallels with the fact that by their nature and function, β-cells are prone to biosynthetic stress with limited measures for self-defense. Beta cell stress may induce an immune attack that has considerable negative effects on the production of a vital hormone, insulin. If then, both β-cell stress and islet autoimmunity can be harnessed as targets for intervention strategies. This also may explain why immunotherapy at best delays the progression of T1D and suggests the use of alternative therapies to expand β-cells, in combination with immune intervention strategies, to reverse the disease. Future research should extend to further investigate β-cell biology, in addition to studies of immunologic areas, to find appropriate biomarkers of T1D susceptibility. This will help to decipher β-cell characteristics and the factors regulating their function to develop novel therapeutic approaches. Full article
(This article belongs to the Special Issue Molecular Mechanism of Diabetic Kidney Disease (2nd Edition))
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27 pages, 1493 KiB  
Review
Autophagy and Mitophagy in Diabetic Kidney Disease—A Literature Review
by Alina Mihaela Stanigut, Liliana Tuta, Camelia Pana, Luana Alexandrescu, Adrian Suceveanu, Nicoleta-Mirela Blebea and Ileana Adela Vacaroiu
Int. J. Mol. Sci. 2025, 26(2), 806; https://doi.org/10.3390/ijms26020806 - 18 Jan 2025
Viewed by 1657
Abstract
Autophagy and mitophagy are critical cellular processes that maintain homeostasis by removing damaged organelles and promoting cellular survival under stress conditions. In the context of diabetic kidney disease, these mechanisms play essential roles in mitigating cellular damage. This review provides an in-depth analysis [...] Read more.
Autophagy and mitophagy are critical cellular processes that maintain homeostasis by removing damaged organelles and promoting cellular survival under stress conditions. In the context of diabetic kidney disease, these mechanisms play essential roles in mitigating cellular damage. This review provides an in-depth analysis of the recent literature on the relationship between autophagy, mitophagy, and diabetic kidney disease, highlighting the current state of knowledge, existing research gaps, and potential areas for future investigations. Diabetic nephropathy (DN) is traditionally defined as a specific form of kidney disease caused by long-standing diabetes, characterized by the classic histological lesions in the kidney, including mesangial expansion, glomerular basement membrane thickening, nodular glomerulosclerosis (Kimmelstiel–Wilson nodules), and podocyte injury. Clinical markers for DN are albuminuria and the gradual decline in glomerular filtration rate (GFR). Diabetic kidney disease (DKD) is a broader and more inclusive term, for all forms of chronic kidney disease (CKD) in individuals with diabetes, regardless of the underlying pathology. This includes patients who may have diabetes-associated kidney damage without the typical histological findings of diabetic nephropathy. It also accounts for patients with other coexisting kidney diseases (e.g., hypertensive nephrosclerosis, ischemic nephropathy, tubulointerstitial nephropathies), even in the absence of albuminuria, such as a reduction in GFR. Full article
(This article belongs to the Special Issue Molecular Mechanism of Diabetic Kidney Disease (2nd Edition))
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17 pages, 932 KiB  
Review
Molecular Targets of Novel Therapeutics for Diabetic Kidney Disease: A New Era of Nephroprotection
by Alessio Mazzieri, Francesca Porcellati, Francesca Timio and Gianpaolo Reboldi
Int. J. Mol. Sci. 2024, 25(7), 3969; https://doi.org/10.3390/ijms25073969 - 3 Apr 2024
Cited by 14 | Viewed by 6871
Abstract
Diabetic kidney disease (DKD) is a chronic microvascular complication in patients with diabetes mellitus (DM) and the leading cause of end-stage kidney disease (ESKD). Although glomerulosclerosis, tubular injury and interstitial fibrosis are typical damages of DKD, the interplay of different processes (metabolic factors, [...] Read more.
Diabetic kidney disease (DKD) is a chronic microvascular complication in patients with diabetes mellitus (DM) and the leading cause of end-stage kidney disease (ESKD). Although glomerulosclerosis, tubular injury and interstitial fibrosis are typical damages of DKD, the interplay of different processes (metabolic factors, oxidative stress, inflammatory pathway, fibrotic signaling, and hemodynamic mechanisms) appears to drive the onset and progression of DKD. A growing understanding of the pathogenetic mechanisms, and the development of new therapeutics, is opening the way for a new era of nephroprotection based on precision-medicine approaches. This review summarizes the therapeutic options linked to specific molecular mechanisms of DKD, including renin-angiotensin-aldosterone system blockers, SGLT2 inhibitors, mineralocorticoid receptor antagonists, glucagon-like peptide-1 receptor agonists, endothelin receptor antagonists, and aldosterone synthase inhibitors. In a new era of nephroprotection, these drugs, as pillars of personalized medicine, can improve renal outcomes and enhance the quality of life for individuals with DKD. Full article
(This article belongs to the Special Issue Molecular Mechanism of Diabetic Kidney Disease (2nd Edition))
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