Evidence map›Paper›PMID 26801305›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2016

Emerging role of hydrogen sulfide-microRNA crosstalk in cardiovascular diseases.

Bryan T Hackfort, Paras K Mishra

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.0field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 45 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. The crucial relationship between miRNA-27 and CSE/HInternational journal of medical sciences · 2024
    Article
  5. Dual targeting of HHeliyon · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. The Cardiovascular Effects of Hydrogen Sulfide: The Epigenetic Mechanisms.Advances in experimental medicine and biology · 2021
    Article
  11. Review
  12. Review
  13. Article
  14. HExperimental and therapeutic medicine · 2019
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Cross-talk of MicroRNA and hydrogen sulfide: A novel therapeutic approach for bone diseases.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2017
    Review
  20. HScientific reports · 2017
    Article
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.

Bryan T HackfortDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; and.
Paras K MishraDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, Nebraska; and Department of Anesthesiology, University of Nebraska Medical Center, Omaha, Nebraska paraskumar.mishra@unmc.edu.
University of Nebraska Medical Center · US

Funding

Inflammation, miRNA and autophagy in diabetesR01HL113281 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MISHRA, PARAS KUMAR · 2013 to 2017
$1.9M
Exercise and H2S mitigate homocysteine-mediated beta2-adrenergic receptor dysfuncR01HL116205 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MISHRA, PARAS KUMAR · 2013 to 2017
$1.9M
NHLBI NIH HHS HL-113281NHLBI NIH HHS HL-116205NHLBI NIH HHS R01 HL113281NHLBI NIH HHS R01 HL116205
6 · The paper itself

Abstract

Despite an obnoxious smell and toxicity at a high dose, hydrogen sulfide (H2S) is emerging as a cardioprotective gasotransmitter. H2S mitigates pathological cardiac remodeling by regulating several cellular processes including fibrosis, hypertrophy, apoptosis, and inflammation. These encouraging findings in rodents led to initiation of a clinical trial using a H2S donor in heart failure patients. However, the underlying molecular mechanisms by which H2S mitigates cardiac remodeling are not completely understood. Empirical evidence suggest that H2S may regulate signaling pathways either by directly influencing a gene in the cascade or interacting with nitric oxide (another cardioprotective gasotransmitter) or both. Recent studies revealed that H2S may ameliorate cardiac dysfunction by up- or downregulating specific microRNAs. MicroRNAs are noncoding, conserved, regulatory RNAs that modulate gene expression mostly by translational inhibition and are emerging as a therapeutic target for cardiovascular disease (CVD). Few microRNAs also regulate H2S biosynthesis. The inter-regulation of microRNAs and H2S opens a new avenue for exploring the H2S-microRNA crosstalk in CVD. This review embodies regulatory mechanisms that maintain the physiological level of H2S, exogenous H2S donors used for increasing the tissue levels of H2S, H2S-mediated regulation of CVD, H2S-microRNAs crosstalk in relation to the pathophysiology of heart disease, clinical trials on H2S, and future perspectives for H2S as a therapeutic agent for heart failure.

Indexed as

Signal TransductionAnimalsCardiovascular DiseasesHumansHydrogen SulfideMicroRNAsHydrogen SulfideMicroRNAsapoptosisclinical trialfibrosisheart failureinflammationmicroRNAs

Identifiers

PMID26801305
PMCPMC4867357
OpenAlexW2300698379

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.