Evidence map›Paper›PMID 41596289›Full record

ReviewInternational journal of molecular sciences2026

Nitric Oxide Signaling in Cardiovascular Physiology and Pathology: Mechanisms, Dysregulation, and Therapeutic Frontiers.

Sakthipriyan Venkatesan, Carlo Smirne, Carmen Imma Aquino, Daniela Surico, Valentino Remorgida, Mohammad Mostafa Ola Pour, Mario Pirisi, Elena Grossini

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2026. 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
–field-weighted citation impact
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.

  1. Review
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  4. Pharmaceuticals (Basel, Switzerland) · 2026
    Review
  5. Review
  6. Article
  7. Review
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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

8 authors.

Sakthipriyan VenkatesanLaboratory of Physiology, Department of Translational Medicine, Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy.ORCID 0000-0002-7517-2574
Carlo SmirneInternal Medicine Unit, Department of Translational Medicine, Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy.ORCID 0000-0002-3338-5416
Carmen Imma AquinoGynecology and Obstetrics Unit, Department of Translational Medicine, Università del Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0002-4797-6161
Daniela SuricoGynecology and Obstetrics Unit, Department of Translational Medicine, Università del Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0001-6801-0043
Valentino RemorgidaGynecology and Obstetrics Unit, Department of Translational Medicine, Università del Piemonte Orientale, 28100 Novara, Italy.ORCID 0000-0002-5043-6676
Mohammad Mostafa Ola PourLaboratory of Physiology, Department of Translational Medicine, Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy.ORCID 0000-0001-8810-4688
Mario PirisiInternal Medicine Unit, Department of Translational Medicine, Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy.ORCID 0000-0001-9740-0155
Elena GrossiniLaboratory of Physiology, Department of Translational Medicine, Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy.ORCID 0000-0002-3012-259X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitric oxide (NO), a fundamental gaseous signaling molecule, is indispensable for cardiovascular homeostasis. This review synthesizes the expansive field of NO biology within the unifying framework of Nitric Oxide Equilibrium (NOE), i.e., the critical balance between its synthesis, bioavailability, and degradation. In a physiological state, NOE maintains vascular health by regulating blood pressure, preventing thrombosis, suppressing inflammation, and optimizing both cardiac and mitochondrial function. Here, we analyze how NOE disruption, primarily through oxidative stress and enzymatic dysfunction, underlies the pathogenesis of major cardiovascular diseases, including atherosclerosis, heart failure, ischemia-reperfusion injury, and cerebrovascular diseases like stroke. A critical evaluation of therapeutic strategies designed to restore NOE is presented, encompassing classic NO donors and phosphodiesterase-5 inhibitors, alongside next-generation soluble guanylate cyclase modulators and precision nanomedicine approaches. By identifying key knowledge gaps and methodological hurdles, this review charts a course for future research focused on biomarker-guided interventions and personalized medicine. Ultimately, we frame the restoration of NOE as a paramount therapeutic goal, crucial to translating decades of molecular research into effective clinical practice.

Indexed as

Cardiovascular DiseasesCardiovascular Physiological PhenomenaCardiovascular SystemNitric OxideSignal TransductionAnimalsHumansOxidative StressNitric Oxidecardiovascular diseaseendothelial dysfunctionnitric oxide equilibriumoxidative stresstherapeutics

Identifiers

PMID41596289
PMCPMC12841060

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.