Molecular mechanism of renal lipid accumulation in diabetic kidney disease DOI Creative Commons

Zhengying Fang,

Ruijie Liu, Jingyuan Xie

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(11)

Published: June 1, 2024

Abstract Diabetic kidney disease (DKD) is a leading cause of end stage renal with unmet clinical demands for treatment. Lipids are essential cell survival; however, cells have limited capability to metabolize overloaded lipids. Dyslipidaemia common in DKD patients and ectopic lipid accumulation associated progression. Unveiling the molecular mechanism involved regulation crucial exploring potential therapeutic targets. In this review, we focused on underlying cholesterol, oxysterol fatty acid metabolism disorder context DKD. Specific regulators different compartment TREM2 macrophages, lipid‐related macrophages DKD, were discussed. The role sodium‐glucose transporter 2 inhibitors improving was summarized.

Language: Английский

Renal tubular epithelial cells response to injury in acute kidney injury DOI Creative Commons
Zuo‐Lin Li, Xinyan Li, Yan Zhou

et al.

EBioMedicine, Journal Year: 2024, Volume and Issue: 107, P. 105294 - 105294

Published: Aug. 23, 2024

Acute kidney injury (AKI) is a clinical syndrome characterized by rapid and significant decrease in renal function that can arise from various etiologies, associated with high morbidity mortality. The tubular epithelial cells (TECs) represent the central cell type affected AKI, their notable regenerative capacity critical for recovery of afflicted patients. adaptive repair process initiated surviving TECs following mild AKI facilitates full recovery. Conversely, when severe or persistent, it allows to undergo pathological responses, abnormal phenotypic transformation, which will lead development fibrosis. Given implications fate after outcomes, deeper understanding these mechanisms necessary identify promising therapeutic targets biomarkers human kidney.

Language: Английский

Citations

14

Renal Mitochondrial ATP Transporter Ablation Ameliorates Obesity-Induced CKD DOI Creative Commons
Anna Permyakova,

Sharleen Hamad,

Liad Hinden

et al.

Journal of the American Society of Nephrology, Journal Year: 2024, Volume and Issue: 35(3), P. 281 - 298

Published: Jan. 11, 2024

Significance Statement This study sheds light on the central role of adenine nucleotide translocase 2 (ANT2) in pathogenesis obesity-induced CKD. Our data demonstrate that ANT2 depletion renal proximal tubule cells (RPTCs) leads to a shift their primary metabolic program from fatty acid oxidation aerobic glycolysis, resulting mitochondrial protection, cellular survival, and preservation function. These findings provide new insights into underlying mechanisms CKD have potential be translated toward development targeted therapeutic strategies for this debilitating condition. Background The impairment ATP production transport RPTCs has been linked condition is characterized by kidney dysfunction, inflammation, lipotoxicity, fibrosis. In study, we investigated ANT2, which serves as regulator content RPTCs, Methods We generated RPTC-specific knockout ( RPTC-ANT2 −/− ) mice, were then subjected 24-week high-fat diet–feeding regimen. conducted comprehensive assessment morphology, function, alterations these mice. addition, used large-scale transcriptomics, proteomics, metabolomics analyses gain regulating RPTC physiology, overall health. Results revealed obese mice displayed preserved morphology along with notable absence lipotoxicity Ant2 led fundamental rewiring program. Specifically, shifted oxidizing acids energy source favoring phenomenon mediated testis-selective Ant4. Conclusions propose significant RPTC-Ant2 nullification triggers cascade mechanisms, including enhanced ultimately shed complex pathways contributing suggest targets

Language: Английский

Citations

10

Immunology of Kidney Disease DOI
Orestes Foresto‐Neto, Luísa Menezes-Silva, Jefferson Antônio Leite

et al.

Annual Review of Immunology, Journal Year: 2024, Volume and Issue: 42(1), P. 207 - 233

Published: Jan. 12, 2024

The immune system and the kidneys are closely related. Immune components mediate acute kidney disease crucial to progression of chronic disease. Beyond its pathogenic functions, supports immunological homeostasis in healthy kidneys. help maintain equilibrium by removing metabolic waste products toxins, thereby limiting local systemic inflammation. In this review, we describe close relationship between We discuss how imbalance response can be deleterious immunomodulation important preventing end-stage renal addition, recent tools such as silico platforms organoids unveil cells homeostasis.

Language: Английский

Citations

10

Cardiometabolic comorbidities and complications of obesity and chronic kidney disease (CKD) DOI Creative Commons

Mariam M. Ali,

Sanober Parveen,

Vanessa Williams

et al.

Journal of Clinical & Translational Endocrinology, Journal Year: 2024, Volume and Issue: 36, P. 100341 - 100341

Published: April 2, 2024

Obesity and chronic kidney disease are two ongoing progressive clinical pandemics of major public health care significance. Because their growing prevalence, indolent course consequent complications both these conditions place significant burden on the delivery system especially in developed countries like United States. Beyond chance coexistence same patient based high prevalence it is now apparent that obesity associated with likely has a direct causal role onset, progression severity disease. The causes underlying pathophysiology this myriad, complicated multi-faceted. In review, continuing theme special edition journal " Cross roads between Endocrinology Nephrology" we review epidemiology related (ORCKD), its various pathophysiology. addition, delve into comorbidities ORCKD particular emphasis cardio metabolic consequences then current body evidence for available strategies modulation as well potential unique weight reduction management improvement risk reduction.

Language: Английский

Citations

9

Molecular mechanism of renal lipid accumulation in diabetic kidney disease DOI Creative Commons

Zhengying Fang,

Ruijie Liu, Jingyuan Xie

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(11)

Published: June 1, 2024

Abstract Diabetic kidney disease (DKD) is a leading cause of end stage renal with unmet clinical demands for treatment. Lipids are essential cell survival; however, cells have limited capability to metabolize overloaded lipids. Dyslipidaemia common in DKD patients and ectopic lipid accumulation associated progression. Unveiling the molecular mechanism involved regulation crucial exploring potential therapeutic targets. In this review, we focused on underlying cholesterol, oxysterol fatty acid metabolism disorder context DKD. Specific regulators different compartment TREM2 macrophages, lipid‐related macrophages DKD, were discussed. The role sodium‐glucose transporter 2 inhibitors improving was summarized.

Language: Английский

Citations

9