Evidence map›Paper›PMID 28217447›Full record

ReviewTranslational andrology and urology2017

Aging related erectile dysfunction-potential mechanism to halt or delay its onset.

Monica G Ferrini, Nestor F Gonzalez-Cadavid, Jacob Rajfer

Open access · hybridAbstract readReview
In one paragraph

Review in Translational andrology and urology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
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  15. The world journal of men's health · 2024
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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

3 authors at 2 institutions in 1 country.

Monica G FerriniDepartment of Health and Life Sciences, Charles R. Drew University of Medicine and Science, Los Angeles, CA, USA.
Nestor F Gonzalez-CadavidDepartment of Urology, UCLA School of Medicine, Los Angeles, CA, USA;; Department of Internal Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA, USA.
Jacob RajferDepartment of Urology, UCLA School of Medicine, Los Angeles, CA, USA.
Charles R. Drew University of Medicine and Science · USUniversity of California, Los Angeles · US

Funding

Sustaining Faculty Development & Community EngagementS21MD000103 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED &SCI · PI CARLISLE, DAVID M · 2001 to 2015
$73.9M
Workshop for Junior Biostatisticians in Health ResearchU54MD007598 · NIMHD · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI Ali Andalibi, Jose A Torres-Ruiz · 2012 to 2026
$60.0M
Nitric Oxide/cGMP Modulation of Corporal Fibrosis Caused by NeuropraxiaSC1NS064611 · NINDS · CHARLES R. DREW UNIVERSITY OF MED & SCI · PI FERRINI, MONICA GABRIELA · 2008 to 2012
$1.4M
NIMHD NIH HHS S21 MD000103NIMHD NIH HHS U54 MD007598NINDS NIH HHS SC1 NS064611
6 · The paper itself

Abstract

Erectile dysfunction (ED) will visit every man at some time in his life. The age at when that knock on the door is heard is totally dependent on one's genetics as well as other extrinsic factors. Unlike guests who come for a visit and then leave, once ED shows up it tends to hang around forever. To add insult to injury, the longer ED hangs around, the worse it will get. It is estimated that by the time a man is in his 40's, he has about a 40% chance of having some form of ED and this prevalence increases about 10% per decade thereafter. This suggests that the aging related process that leads to ED begins early in life. It turns out that the most common cause of ED, regardless of the patient's age, is due to a problem with the vascular system of the penis. However, this specific aging related vascular problem is not caused by arterial disease but due to a dysfunction and/or loss of the corporal smooth muscle cells (SMC), the main constituent of the corporal sinusoids. As one gets older, these SMC continue to degrade and disappear. When approximately 15% of these cells have been impacted, it results in an inability of the corporal tissue to retain and/or prevent the blood from "leaking" out of the corporal sinusoids into the systemic veins. However, the corporal SMC themselves begin to combat this aging process by expressing the inducible nitric oxide synthase (iNOS) enzyme to make nitric oxide (NO) in an attempt to quench the high intracellular oxidative stress responsible for the SMC apoptosis. When this iNOS pathway is then pharmacologically upregulated, reversal of these aging related changes in the corpora with correction of the venous leakage is observed. Since we believe that aging related ED is pathologically the same disorder as essential hypertension, the development of a therapeutic regimen that can halt, delay or possibly reverse the cellular processes that lead to aging related ED should also be applicable to those patients diagnosed with essential hypertension.

Indexed as

agingErectile dysfunction (ED)inducible nitric oxide synthase (iNOS)nitric oxide (NO)

Identifiers

PMID28217447
PMCPMC5313305
OpenAlexW2586544529

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.