What does this research mean for the field?

Angiotensin II, acting through the AT1a receptor, plays a pathogenic role in immune-mediated renal injuries by exacerbating glomerular MCP-1 expression and promoting subsequent tissue damage. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To elucidate the role of angiotensin II and its type 1a receptor in immune-mediated renal injury using an experimental model of anti-glomerular basement membrane nephritis.

March 1, 1999Journal of Clinical InvestigationOpen Access

Angiotensin II plays a pathogenic role in immune-mediated renal injury in mice

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Why the study?

Does AT1a deficiency ameliorate immune-mediated renal injury in mice with anti-GBM nephritis?

Population

Angiotensin II type 1a receptor-deficient homozygous and wild-type mice with anti-glomerular basement…

Comparison

AT1a deficiency (genetic knockout) vs Wild-type (AT1a+/+) mice

Design

Preclinical

Follow-up

up to 14 days

Authors

YHYutaka HisadaMitsubishi Chemical (Japan)TSTakeshi SugayaSt. Marianna University School of Medicine MYMasaya YamanouchiMitsubishi Group (Japan)

Discussion

Member takes

Implication

AT1a targeting may mitigate immune glomerular injury; leaves open translation to human anti-GBM disease.

Key Points

To elucidate the role of angiotensin II and its type 1a receptor in immune-mediated renal injury using an experimental model of anti-glomerular basement membrane nephritis.
Induced anti-glomerular basement membrane (GBM) nephritis in angiotensin II type 1a receptor-deficient (AT1a-/-) and wild-type (AT1a+/+) mice.
Tracked renin-angiotensin system activation, renal expression of MCP-1, TGF-beta1, and collagen type I, as well as proteinuria and histological tissue damage over 14 days.
Wild-type mice showed secondary exacerbation of glomerular MCP-1 expression at days 7 and 14 following initial renin-angiotensin system activation, leading to severe proteinuria, elevated TGF-beta1 and collagen type I, glomerulosclerosis, and interstitial fibrosis.
AT1a-deficient mice displayed marked amelioration of glomerular MCP-1 expression, severe proteinuria, and chronic renal structural damage.

Structured PICO

Does AT1a deficiency ameliorate immune-mediated renal injury in mice with anti-GBM nephritis?

Population

Angiotensin II type 1a receptor (AT1a)-deficient homozygous (AT1a-/-) and wild-type (AT1a+/+) mice with anti-glomerular basement membrane (GBM) nephritis

Intervention

AT1a deficiency (genetic knockout)

Comparator

Wild-type (AT1a+/+) mice

Outcome

Renal injury (proteinuria, tissue damage, glomerulosclerosis, interstitial fibrosis, MCP-1 expression)surrogate

Angiotensin II, mediated by AT1a, plays a pathogenic role in immune-mediated renal injury by exacerbating glomerular MCP-1 expression.

Cite This Study

Hisada et al. (1999) studied this question.

synapsesocial.com/papers/6a1e774e20458ccdef55e83d https://doi.org/10.1172/jci2454

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Angiotensin II plays a pathogenic role in immune-mediated renal injury in mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Angiotensin II plays a pathogenic role in immune-mediated renal injury in mice

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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