Evidence map›Paper›PMID 34533692›Full record

ReviewCardiovascular drugs and therapy2022

Prolyl Hydroxylase Inhibitors: a New Opportunity in Renal and Myocardial Protection.

Juan Antonio Requena-Ibáñez, Carlos G Santos-Gallego, Anderly Rodriguez-Cordero, M Urooj Zafar, Juan José Badimon

Abstract readReview
PubMed Publisher
In one paragraph

Review in Cardiovascular drugs and therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 22 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Juan Antonio Requena-IbáñezAtherothrombosis Research Unit, Icahn School of Medicine At Mount Sinai, One Gustave L. Levy Pl, New York, NY, 10029-0310, USA.
Carlos G Santos-GallegoAtherothrombosis Research Unit, Icahn School of Medicine At Mount Sinai, One Gustave L. Levy Pl, New York, NY, 10029-0310, USA.
Anderly Rodriguez-CorderoAtherothrombosis Research Unit, Icahn School of Medicine At Mount Sinai, One Gustave L. Levy Pl, New York, NY, 10029-0310, USA.
M Urooj ZafarAtherothrombosis Research Unit, Icahn School of Medicine At Mount Sinai, One Gustave L. Levy Pl, New York, NY, 10029-0310, USA.
Juan José BadimonAtherothrombosis Research Unit, Icahn School of Medicine At Mount Sinai, One Gustave L. Levy Pl, New York, NY, 10029-0310, USA. Juan.Badimon@mssm.edu.ORCID 0000-0002-6780-8771
Icahn School of Medicine at Mount Sinai · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia, via the activity of hypoxia-inducible factors (HIFs), plays a crucial role in fibrosis, inflammation, and oxidative injury, processes which are associated with progression of cardiovascular and kidney diseases. HIFs are key transcription heterodimers consisting of regulatory α-subunits (HIF-1α, HIF-2α, HIF-3α) and a constitutive β-subunit (HIF-β). The stability of HIFs is regulated by the prolyl hydroxylases (PHDs). Specific PHD inhibitors (PHD-i) are being investigated as a therapeutic approach to modulate the cellular signaling pathways and harness the native protective adaptive responses to hypoxia. Selective inhibition of PHD leads to the stabilization of the HIFs, which is the transcriptional gatekeeper of a multitude of genes involved in angiogenesis, energy metabolism, apoptosis, inflammation, and fibrosis. PHD-i downregulate hepcidin, improve iron absorption, and increase the endogenous production of erythropoietin. Furthermore, this pharmacological group has also been proven to ameliorate ischemic injuries in several organs, opening a new and promising field in cardiovascular research.. In this review, we present the basic and clinical potential of PHD-i treatment in different scenarios, such as ischemic heart disease, cardiac hypertrophy and heart failure, and their interplay with other pharmacological agents with proven cardiovascular benefits, such as sodium-glucose cotransporter 2 (SGLT2) inhibitors.

Indexed as

Prolyl-Hydroxylase InhibitorsFibrosisHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitInflammationProlyl HydroxylasesHypoxia-Inducible Factor 1, alpha SubunitProlyl-Hydroxylase InhibitorsProlyl HydroxylasesCardiovascular diseaseChronic kidney diseaseHeart failureHypoxiaHypoxia-inducible factorProlyl hydroxylase inhibitors

Identifiers

PMID34533692
OpenAlexW3200690449

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.