Evidence map›Paper›PMID 37953501›Full record

ReviewCNS neuroscience & therapeutics2024

Role of brain renin-angiotensin system in depression: A new perspective.

Naif H Ali, Hayder M Al-Kuraishy, Ali I Al-Gareeb, Ali K Albuhadily, Rabab S Hamad, Athanasios Alexiou, Marios Papadakis, Hebatallah M Saad, Gaber El-Saber Batiha

Erratum issuedOpen access · goldAbstract readReview
In one paragraph

Review in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 29 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 2 pooled it
3.5field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 2 syntheses or guidelines pooled it, 36 citations in OpenAlex.

  1. Pooled it
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  6. Ang II-mediated effects on BBB integrity in psychiatric and neurological disorders.Progress in neuro-psychopharmacology & biological psychiatry · 2026
    Review
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  10. Comparative Study on the Neuroprotective Effects of Perindopril and Benazepril in Experimentally-induced Chronic Mild Stress in Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 7 institutions in 5 countries.

Naif H AliDepartment of Internal Medicine, Medical College, Najran University, Najran, KSA.
Hayder M Al-KuraishyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Ali I Al-GareebDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Ali K AlbuhadilyDepartment of Clinical Pharmacology and Medicine, College of Medicine, Mustansiriyah University, Baghdad, Iraq.
Rabab S HamadBiological Sciences Department, College of Science, King Faisal University, Al Ahsa, Saudi Arabia.ORCID 0000-0002-3465-4470
Athanasios AlexiouUniversity Centre for Research & Development, Chandigarh University, Mohali, Punjab, India.ORCID 0000-0002-2206-7236
Marios PapadakisDepartment of Surgery II, University Hospital Witten-Herdecke, University of Witten-Herdecke, Wuppertal, Germany.
Hebatallah M SaadDepartment of Pathology, Faculty of Veterinary Medicine, Matrouh University, Matrouh, Egypt.ORCID 0000-0001-9555-7300
Gaber El-Saber BatihaDepartment of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour, AlBeheira, Egypt.
Mustansiriyah University · IQChandigarh University · INDamanhour University · EGEgypt Nanotechnology Center · EGKing Faisal University · SANajran University · SAWitten/Herdecke University · DE

Funding

University of Witten-Herdecke Germany
6 · The paper itself

Abstract

Depression is a mood disorder characterized by abnormal thoughts. The pathophysiology of depression is related to the deficiency of serotonin (5HT), which is derived from tryptophan (Trp). Mitochondrial dysfunction, oxidative stress, and neuroinflammation are involved in the pathogenesis of depression. Notably, the renin-angiotensin system (RAS) is involved in the pathogenesis of depression, and different findings revealed that angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) may be effective in depression. However, the underlying mechanism for the role of dysregulated brain RAS-induced depression remains speculative. Therefore, this review aimed to revise the conceivable role of ACEIs and ARBs and how these agents ameliorate the pathophysiology of depression. Dysregulation of brain RAS triggers the development and progression of depression through the reduction of brain 5HT and expression of brain-derived neurotrophic factor (BDNF) and the induction of mitochondrial dysfunction, oxidative stress, and neuroinflammation. Therefore, inhibition of central classical RAS by ARBS and ACEIs and activation of non-classical RAS prevent the development of depression by regulating 5HT, BDNF, mitochondrial dysfunction, oxidative stress, and neuroinflammation.

Indexed as

Angiotensin-Converting Enzyme InhibitorsMitochondrial DiseasesAngiotensin Receptor AntagonistsBrain-Derived Neurotrophic FactorDepressionHumansNeuroinflammatory DiseasesRenin-Angiotensin SystemAngiotensin-Converting Enzyme InhibitorsAngiotensin Receptor AntagonistsBrain-Derived Neurotrophic Factorangiotensinangiotensin‐converting enzyme inhibitorsangiotensin receptor blockersdepressionrenin–angiotensin system

Identifiers

PMID37953501
PMCPMC11017442
OpenAlexW4388635795

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.