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NOX5 and Mitochondrial Dysfunction in Diabetic Nephropathy
Student Name
Student ID
Subject Name
Learning Facilitator
, 2
Title: “NOX5 and Mitochondrial Dysfunction in Diabetic Nephropathy”
Understanding Diabetic Nephropathy
Diabetic nephropathy (DN), a leading cause of end-stage renal disease (ESRD), is one of
the most severe and costly complications of both type 1 and type 2 diabetes mellitus.
Characterized by persistent albuminuria, declining glomerular filtration rate (GFR), and
increased blood pressure, DN significantly impairs kidney function and quality of life (Jha et al.,
2022). The condition develops over the years, progressing through stages of microalbuminuria to
overt proteinuria and eventually leading to renal fibrosis and failure. With global diabetes
prevalence on the rise, DN is becoming increasingly burdensome in both developing and
developed healthcare systems.
Traditionally, the focus has been on hyperglycemia-induced damage to glomerular cells,
but recent advances have shifted attention to molecular and mitochondrial mechanisms involved
in disease progression. Mitochondrial dysfunction and oxidative stress have emerged as key
contributors to renal injury. These cellular disruptions impair energy homeostasis and lead to the
generation of reactive oxygen species (ROS), which damage the glomeruli, tubules, and vascular
components of the kidney (Wang et al., 2021). Recently, NOX5 has become a focus of interest
because it is believed to contribute to diabetic nephropathy. Unlike other NOX forms, NOX5 is
managed by calcium and tied to inflammation, fibrosis, and mitochondrial damage, according to
recent studies by Jandeleit-Dahm et al. (2024) and Zhang et al. (2024). Overactive NOX5 in
kidney cells may bring about inflammation and fibrosis, so it is currently being considered for
therapy in DN (Jha et al., 2023). Investigating how NOX5 and mitochondria influence DN opens
up a fresh opportunity for designing medications that can stop or reverse kidney damage in
people with diabetes.
NOX5 and Mitochondrial Dysfunction in Diabetic Nephropathy
Student Name
Student ID
Subject Name
Learning Facilitator
, 2
Title: “NOX5 and Mitochondrial Dysfunction in Diabetic Nephropathy”
Understanding Diabetic Nephropathy
Diabetic nephropathy (DN), a leading cause of end-stage renal disease (ESRD), is one of
the most severe and costly complications of both type 1 and type 2 diabetes mellitus.
Characterized by persistent albuminuria, declining glomerular filtration rate (GFR), and
increased blood pressure, DN significantly impairs kidney function and quality of life (Jha et al.,
2022). The condition develops over the years, progressing through stages of microalbuminuria to
overt proteinuria and eventually leading to renal fibrosis and failure. With global diabetes
prevalence on the rise, DN is becoming increasingly burdensome in both developing and
developed healthcare systems.
Traditionally, the focus has been on hyperglycemia-induced damage to glomerular cells,
but recent advances have shifted attention to molecular and mitochondrial mechanisms involved
in disease progression. Mitochondrial dysfunction and oxidative stress have emerged as key
contributors to renal injury. These cellular disruptions impair energy homeostasis and lead to the
generation of reactive oxygen species (ROS), which damage the glomeruli, tubules, and vascular
components of the kidney (Wang et al., 2021). Recently, NOX5 has become a focus of interest
because it is believed to contribute to diabetic nephropathy. Unlike other NOX forms, NOX5 is
managed by calcium and tied to inflammation, fibrosis, and mitochondrial damage, according to
recent studies by Jandeleit-Dahm et al. (2024) and Zhang et al. (2024). Overactive NOX5 in
kidney cells may bring about inflammation and fibrosis, so it is currently being considered for
therapy in DN (Jha et al., 2023). Investigating how NOX5 and mitochondria influence DN opens
up a fresh opportunity for designing medications that can stop or reverse kidney damage in
people with diabetes.
