What question did this study set out to answer?

To delineate the biomarkers, pathophysiological mechanisms, and key signaling pathways driving the transition from acute kidney injury and acute kidney disease to chronic kidney disease.

February 1, 2024International Journal of Molecular SciencesOpen Access

From Acute to Chronic: Unraveling the Pathophysiological Mechanisms of the Progression from Acute Kidney Injury to Acute Kidney Disease to Chronic Kidney Disease

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Authors

TYTzu-Hsuan Yeh KTKuan-Chieh Tu HWHsien‐Yi Wang

Discussion

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Overview

Review uncovers molecular pathways driving acute-to-chronic kidney injury progression, highlighting the therapeutic potential of renin-angiotensin system inhibition.

Key Points

To delineate the biomarkers, pathophysiological mechanisms, and key signaling pathways driving the transition from acute kidney injury and acute kidney disease to chronic kidney disease.
Categorized acute kidney injury biomarkers across functional, damage, and stress classifications for clinical utility.
Synthesized molecular and cellular mechanisms of kidney damage progression, including hypoperfusion, sepsis, nephrotoxicity, and immune response.
Identified inflammation, hypoxia, mitochondrial dysfunction, cellular senescence, and key cascades—such as Wnt/β-catenin, TGF-β/SMAD, and Hippo/YAP/TAZ—as critical drivers of maladaptive repair and renal fibrosis.
Highlighted the renin-angiotensin-aldosterone system as a major promoter of oxidative stress and fibrotic changes leading to chronic kidney disease.
Observed qualitative clinical evidence supporting the use of renin-angiotensin system inhibitors to attenuate disease progression post-injury, pending larger trial confirmation.

Cite This Study

Yeh et al. (2024) studied this question.

synapsesocial.com/papers/69da22711e2c7d7b4fa3bfd9 https://doi.org/10.3390/ijms25031755

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February 1, 2024International Journal of Molecular SciencesOpen Access

From Acute to Chronic: Unraveling the Pathophysiological Mechanisms of the Progression from Acute Kidney Injury to Acute Kidney Disease to Chronic Kidney Disease

View Full Paper

Ask AI

Bookmark

Authors

TYTzu-Hsuan Yeh KTKuan-Chieh Tu HWHsien‐Yi Wang

Discussion

Member takes

Overview

Review uncovers molecular pathways driving acute-to-chronic kidney injury progression, highlighting the therapeutic potential of renin-angiotensin system inhibition.

Key Points

To delineate the biomarkers, pathophysiological mechanisms, and key signaling pathways driving the transition from acute kidney injury and acute kidney disease to chronic kidney disease.
Categorized acute kidney injury biomarkers across functional, damage, and stress classifications for clinical utility.
Synthesized molecular and cellular mechanisms of kidney damage progression, including hypoperfusion, sepsis, nephrotoxicity, and immune response.
Identified inflammation, hypoxia, mitochondrial dysfunction, cellular senescence, and key cascades—such as Wnt/β-catenin, TGF-β/SMAD, and Hippo/YAP/TAZ—as critical drivers of maladaptive repair and renal fibrosis.
Highlighted the renin-angiotensin-aldosterone system as a major promoter of oxidative stress and fibrotic changes leading to chronic kidney disease.
Observed qualitative clinical evidence supporting the use of renin-angiotensin system inhibitors to attenuate disease progression post-injury, pending larger trial confirmation.

Cite This Study

Yeh et al. (2024) studied this question.

synapsesocial.com/papers/69da22711e2c7d7b4fa3bfd9 https://doi.org/10.3390/ijms25031755

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