Evidence map›Paper›PMID 36875897›Full record

ReviewJACC. CardioOncology2023

Cardiovascular Toxicity of Proteasome Inhibitors: Underlying Mechanisms and Management Strategies:

Georgios Georgiopoulos, Nikolaos Makris, Ageliki Laina, Foteini Theodorakakou, Alexandros Briasoulis, Ioannis P Trougakos, Meletios-Athanasios Dimopoulos, Efstathios Kastritis, Kimon Stamatelopoulos

Open access · goldAbstract readReview
In one paragraph

Review in JACC. CardioOncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
26.4field-weighted citation impact, top 1% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 91 citations in OpenAlex.

  1. Pooled it
  2. Review
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  5. Observational
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  7. Recent updates and perspectives in "Onco-hypertension".Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Review
  8. Article
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  19. Caught in the crossfire: cardiac complications of cancer therapy.The Journal of clinical investigation · 2026
    Review
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13 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 2 countries.

Georgios GeorgiopoulosDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Nikolaos MakrisDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Ageliki LainaDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Foteini TheodorakakouDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Alexandros BriasoulisDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Ioannis P TrougakosDepartment of Cell Biology and Biophysics, Faculty of Biology, National and Kapodistrian University of Athens, Greece.
Meletios-Athanasios DimopoulosDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Efstathios KastritisDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
Kimon StamatelopoulosDepartment of Clinical Therapeutics, School of Medicine, National and Kapodistrian University of Athens, Athens, Greece.
National and Kapodistrian University of Athens · GRKing's College London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Proteasome inhibitors (PIs) are the backbone of combination treatments for patients with multiple myeloma and AL amyloidosis, while also indicated in Waldenström's macroglobulinemia and other malignancies. PIs act on proteasome peptidases, causing proteome instability due to accumulating aggregated, unfolded, and/or damaged polypeptides; sustained proteome instability then induces cell cycle arrest and/or apoptosis. Carfilzomib, an intravenous irreversible PI, exhibits a more severe cardiovascular toxicity profile as compared with the orally administered ixazomib or intravenous reversible PI such as bortezomib. Cardiovascular toxicity includes heart failure, hypertension, arrhythmias, and acute coronary syndromes. Because PIs are critical components of the treatment of hematological malignancies and amyloidosis, managing their cardiovascular toxicity involves identifying patients at risk, diagnosing toxicity early at the preclinical level, and offering cardioprotection if needed. Future research is required to elucidate underlying mechanisms, improve risk stratification, define the optimal management strategy, and develop new PIs with safe cardiovascular profiles.

Indexed as

ACE, angiotensin-converting enzymeACS, acute coronary syndromeAE, adverse eventAF, atrial fibrillationARB, angiotensin receptor blockerASCT, autologous stem cell transplantationbortezomibBP, blood pressurecardiovascular toxicitycarfilzomibCVAE, cardiovascular adverse eventeNOS, endothelial nitric oxide synthaseESC, European Society of CardiologyFMD, flow-mediated dilatationGLS, global longitudinal strainHF, heart failureHFpEF, heart failure with preserved ejection fractionIHD, ischemic heart diseaseIMiD, immunomodulatory drugixazomibKd, carfilzomib and dexamethasoneLA, left atrialLVEF, left ventricular ejection fractionLV, left ventricularMM, multiple myelomaNO, nitric oxideNP, natriuretic peptideOS, overall survivalPBMC, peripheral blood mononuclear cellPFS, progression-free survivalPH, pulmonary hypertensionPI, proteasome inhibitorPrA, proteasome activityproteasome inhibitionPWV, pulse wave velocityRRMM, relapse or refractory multiple myelomaSBP, systolic blood pressureTMA, thrombotic microangiopathyUPP, ubiquitin proteasome pathwayVd, bortezomib and dexamethasoneVTE, venous thromboembolismWM, Waldenström’s macroglobulinemia

Identifiers

PMID36875897
PMCPMC9982226
OpenAlexW4321502975

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.