Evidence map›Paper›PMID 31632513›Full record

ReviewAmerican journal of translational research2019

RhoA/ROCK pathway: implication in osteoarthritis and therapeutic targets.

Zhenhan Deng, Yiming Jia, Haifeng Liu, Miao He, Yuntao Yang, Wenfeng Xiao, Yusheng Li

Open access · greenAbstract readReview
PubMed Full text at PMC
In one paragraph

Review in American journal of translational research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
6.4field-weighted citation impact, top 3% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  5. Venom-Derived Proteins fromInternational journal of molecular sciences · 2026
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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

7 authors at 3 institutions in 2 countries.

Zhenhan DengDepartment of Orthopedics, Xiangya Hospital, Central South University Changsha 410008, Hunan, China.
Yiming JiaDepartment of Orthopedics, Chifeng Municipal Hospital, Chifeng Clinical Medical School of Inner Mongolia Medical University Chifeng 024000, Inner Mongolia, China.
Haifeng LiuDepartment of Sports Medicine, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital Shenzhen 518035, Guangdong, China.
Miao HeDepartment of Orthopedics, Xiangya Hospital, Central South University Changsha 410008, Hunan, China.
Yuntao YangDepartment of Orthopedics, Xiangya Hospital, Central South University Changsha 410008, Hunan, China.
Wenfeng XiaoDepartment of Orthopedics, Xiangya Hospital, Central South University Changsha 410008, Hunan, China.
Yusheng LiDepartment of Orthopedics, Xiangya Hospital, Central South University Changsha 410008, Hunan, China.
Central South University · CNChifeng Municipal Hospital · CNShenzhen Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ras homolog gene family, member A (RhoA) and its downstream effector Rho-associated protein kinase (ROCK) play important roles in multiple cellular processes, but abnormal activation of this pathway have been reported to be involved in various types of diseases, including osteoarthritis (OA). This article focused to review the RhoA/ROCK association and its functional role in OA development, and possible therapeutics of OA by targeting this pathway. We have explored the databases like Pubmed, Google Scholar, Web of Science and SCOPUS, and collected the papers on Rho/ROCK and their relationship with OA, and reviewed comprehensively. Studies revealed that the abnormal activation of RhoA/ROCK signaling is involved in early phase response to abnormal mechanical stimuli, which is thought to be a contributory factor to OA progression. RhoA/ROCK interacts with OA pathological factors and induces cartilage degeneration through the degradation of chondrocyte extracellular matrix (ECM). As the RhoA/ROCK activity can affect bone formation by triggering cartilage degradation, it may represent a possible therapeutic target to treat OA. Interestingly, several pharmaceutical companies are investing in the development of RhoA/ROCK inhibitors for the treatment of OA. However, a few in vivo experiments have been successfully conducted to demonstrate the potential value of RhoA/ROCK pathway inhibition in the treatment of OA. This review provides an insight into the functional role of Rho/ROCK pathway, and indicates that targeting this pathway might be promising in future OA treatment.

Indexed as

cartilage degenerationosteoarthritisRas homolog gene familyRhoA inhibitorRho-associated protein kinaseROCK inhibitor

Identifiers

PMID31632513
PMCPMC6789288
OpenAlexW2984560320

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.