Evidence map›Paper›PMID 18729731›Full record

ReviewAnnual review of medicine2009

The treatment of hyperhomocysteinemia.

Bradley A Maron, Joseph Loscalzo

Open access · greenAbstract readReview
In one paragraph

Review in Annual review of medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 133 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
133citing papers in PubMed, 3 pooled it
8.6field-weighted citation impact, top 2% 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

133 citing papers in PubMed, 3 syntheses or guidelines pooled it, 310 citations in OpenAlex.

  1. Homocysteine-lowering interventions for preventing cardiovascular events.The Cochrane database of systematic reviews · 2017
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Hyperhomocysteinaemia and chronic venous ulcers.International wound journal · 2015
    Trial
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Pathophysiology of homocysteine: insights into ion channel dysfunction.Pflugers Archiv : European journal of physiology · 2026
    Review
  12. Review
  13. Review
  14. Review
  15. Association of plasma homocysteine with morning blood pressure in patients with essential hypertension.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
    Article
  16. Homocysteine: Canary in the Coal Mine or Hidden Threat? A Biochemical Study on the Role of Plasma Thiols.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  17. Review
  18. Article
  19. Review
  20. Article

73 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

2 authors at 1 institution in 1 country.

Bradley A MaronCardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. bmaron@partners.org
Joseph Loscalzo
Harvard University · US

Funding

Redox regulation in Endothelial Progenitor CellsP01HL081587 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HAMBURG, NAOMI MIRIAM · 2005 to 2015
$21.5M
GPx-3 and Peroxide Flux in the Endothelial CellR37HL061795 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LOSCALZO, JOSEPH · 2007 to 2016
$4.3M
HOMOCYST(E)INE, OXIDATIVE STRESS, AND NITRIC OXIDER01HL058976 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LOSCALZO, JOSEPH · 1997 to 2004
$1.6M
PLATELET DERIVED REACTIVE OXYGEN SPECIES AND PLAQUER01HL061795 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI LOSCALZO, JOSEPH · 1998 to 2006
$1.6M
NHLBI PROTEOMICS INITIATIVE-N01HV28178N01HV028178 · HV · BOSTON UNIVERSITY MEDICAL CAMPUS · PI COSTELLO, CATHERINE E. · 2002 to 2006
–
NHLBI NIH HHS HL58976NHLBI NIH HHS HL61795NHLBI NIH HHS N01 HV028178NHLBI NIH HHS P01 HL081587NHLBI NIH HHS P01HL81587NHLBI NIH HHS R01 HL058976NHLBI NIH HHS R01 HL061795NHLBI NIH HHS R37 HL061795
6 · The paper itself

Abstract

The unique biochemical profile of homocysteine is characterized by chemical reactivity supporting a wide range of molecular effects and by a tendency to promote oxidant stress-induced cellular toxicity. Numerous epidemiological reports have established hyperhomocysteinemia as an independent risk factor for cardiovascular disease, cerebrovascular disease, dementia-type disorders, and osteoporosis-associated fractures. Although combined folic acid and B-vitamin therapy substantially reduces homocysteine levels, results from randomized placebo-controlled clinical trials testing the effect of vitamin therapy on outcome in these diseases have generally fallen short of expectations. These results have led some to abandon homocysteine monitoring in the management of patients with cardiovascular or cognitive disorders. These trials, however, have generally included patients with only mildly elevated homocysteine levels and have not addressed several clinical scenarios in which homocysteine reduction may be effective, including the primary prevention of atherothrombotic disease in individuals at low or intermediate risk, or those with severe hyperhomocysteinemia.

Indexed as

Central Nervous System DiseasesCognition DisordersHumansHyperhomocysteinemia

Identifiers

PMID18729731
PMCPMC2716415
OpenAlexW2153648772

What OpenQuestion holds

Textmetadata
LicenceTDM
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.