Traditional Chinese Medicine (TCM) has demonstrated promising efficacy in managing and preventing the early‑stage diabetic nephropathy (DN). Although the exact mechanisms remain elusive, clinical evidence has suggested that Jinlida granules (JLD) are beneficial in improving renal function among patients with DN. The present study aimed to elucidate the effect of JLD on DN and the underlying molecular mechanism. Therefore, podocyte apoptosis was evaluated using flow cytometry and TUNEL staining, while mitochondrial morphology and function were assessed using transmission electron microscopy, MitoTracker, JC‑1 and reactive oxygen species staining. RNA sequencing analysis was performed to elucidate the mechanism underlying the effect of JLD on DN. Additionally, to investigate the role of peroxisome proliferator‑activated receptor‑γ co‑activator‑1α (PGC‑1α) in mitigating JLD‑induced mitochondrial dysfunction and podocyte apoptosis, MPC5 cells were transfected with the corresponding small interfering RNA constructs. The results showed that JLD effectively improved renal function and mitigated podocyte injury, as well as ameliorated mitochondrial dysfunction and inhibited apoptosis in db/db mice. In vitro experiments further revealed that JLD exerted a protective effect via inhibiting mitochondrial fission and apoptosis in high glucose‑treated podocytes. Furthermore, JLD enhanced the phosphorylation of adenosine monophosphate‑activated protein kinase (AMPK), thus promoting the expression of PGC‑1α, eventually improving apoptosis and mitochondrial homeostasis. Overall, the current study revealed that JLD could improve mitochondrial homeostasis and reduce cell apoptosis in podocytes via activating the AMPK/PGC‑1α pathway, thus providing a theoretical foundation for the clinical management of DN.

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by arterial and/or venous thrombosis, pathological pregnancies and persistent antiphospholipid antibodies. The occurrence and development of APS are complex and associated with immune disorders, with its prognosis remaining uncertain. Owing to its pathogenesis, anticoagulation therapy is the primary treatment for patients with APS. In recent years, with increased attention on APS, research on its treatment strategies has flourished, and preclinical and clinical relevance studies are being conducted to re‑evaluate the mechanism of action of existing drugs and to develop new drugs. Recent evidence suggests that vitamin D (VD) may help improve immune disorders in patients with APS by regulating the balance between immune cells. In this review, the potential mechanistic role of VD in APS protection was discussed, highlighting the potential effects of VD as a promising adjuvant treatment option for APS.

N6‑methyladenosine (m6A) is one of the most universal, abundant and conserved types of internal post‑transcriptional modifications in eukaryotic RNA, and is involved in nuclear RNA export, RNA splicing, mRNA stability, gene expression, microRNA biogenesis and long non‑coding RNA metabolism. AlkB homologue 5 (ALKBH5) acts as a m6A demethylase to regulate a wide variety of biological processes closely associated with tumour progression, tumour metastasis, tumour immunity and tumour drug resistance. ALKBH5 serves a crucial role in human digestive system tumours, mainly through post‑transcriptional regulation of m6A modification. The present review discusses progress in the study of the m6A demethylase ALKBH5 in gastrointestinal tract cancer, summarizes the potential molecular mechanisms of ALKBH5 dysregulation in gastrointestinal tract cancer, and discusses the significance of ALKBH5‑targeted therapy, which may provide novel ideas for future clinical prognosis prediction, biomarker identification and precise treatment.

Following the publication of the above article, an interested reader drew to the Editor's attention that various of the histological structural images shown in Fig. 5 on p. 190 were strikingly similar to data that were featured in Fig. 1A of a previous paper by the same research group that appeared in the Journal Laboratory Animal Research. On re‑examining their original data, the authors confirmed that an error occurred during the paper submission/production process, and that Fig. 5 did not appear in the above article as the authors had intended. The correct version of Fig. 5, containing the data that the authors intended for inclusion in this article, is shown on the next page. Also shown is a corrected version of Table II corresponding to the replacement version of Fig. 5, containing data that are derived from an analysis of the data shown in this figure. Furthermore, the replacement of the images in Fig. 5, and the revisions of the data made in Table II, also dictate that the following changes are needed to be made in the main text of the paper (all associated with Results section on p. 191, 'Recovery effect of EtRLP on histological alterations of the transverse colon' subsection): The sentences in lines 9‑14 of this section should now read as following (changes from the original text are highlighted in bold): 'Following Lop+EtRLP or Lop+Bisac treatments, the villus length increased by 270‑290% relative to the Lop+Vehicle‑treated group (Fig. 5 and Table II). Furthermore, the alterations in muscle thickness were similar to those in villus length, although crypt layer thickness only increased by 145‑150% relative to the Lop+Vehicle‑treated group (Fig. 5 and Table II)'. Note that the errors made during the assembly of Fig. 5 and Table II did not grossly affect the overall conclusions reported in the paper. All the authors agree with the publication of this corrigendum, and are grateful to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this. They also apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 43: 185‑198, 2019; DOI: 10.3892/ijmm.2018.3960].

Colorectal cancer (CRC), an emerging public health concern, is one of the leading causes of cancer morbidity and mortality worldwide. An increasing body of evidence shows that dysfunction in metabolic reprogramming is a crucial characteristic of CRC progression. Specifically, metabolic reprogramming abnormalities in glucose, glutamine and lipid metabolism provide the tumour with energy and nutrients to support its rapid cell proliferation and survival. More recently, microRNAs (miRNAs) appear to be involved in the pathogenesis of CRC, including regulatory roles in energy metabolism. In addition, it has been revealed that dysbiosis in CRC might play a key role in impairing the host metabolic reprogramming processes, and while the exact interactions remain unclear, the link may lie with miRNAs. Hence, the aims of the current review include first, to delineate the metabolic reprogramming abnormalities in CRC; second, to explain how miRNAs mediate the aberrant regulations of CRC metabolic pathways; third, linking miRNAs with metabolic abnormalities and dysbiosis in CRC and finally, to discuss the roles of miRNAs as potential biomarkers.

Cold‑inducible RNA‑binding protein (CIRP) is a cold shock protein implicated in the regulation of multiple biological processes depending on its cellular localization. However, to the best of our knowledge, the role of CIRP in liver regeneration and injury after hepatectomy has not been investigated. The present study was therefore designed to explore whether CIRP is involved in liver regeneration after hepatectomy and its specific role and underlying molecular mechanism. The overall involvement of CIRP in liver regeneration and injury after hepatectomy was evaluated in CIRP‑deficient mice. C23, an antagonist of extracellular CIRP, was used to assess the effect of extracellular CIRP on liver regeneration and injury after hepatectomy. CIRP overexpression and short hairpin RNA plasmids were transfected into HepG2 cells to study the effect of intracellular CIRP on cell proliferation. The effects of extracellular CIRP on cell proliferation and injury were determined via the use of recombinant CIRP protein to stimulate HepG2 cells in vitro. The results indicated that both hepatic and serum CIRP levels significantly increased after partial hepatectomy. Additionally, CIRP deficiency impaired liver regeneration but alleviated liver injury after partial hepatectomy in mice. C23 administration attenuated liver injury and suppressed endoplasmic reticulum (ER) stress and oxidative stress. Loss‑ and gain‑of‑function analyses in HepG2 cells indicated that an increase in intracellular CIRP promoted cell proliferation via signal transducers and activation of transcription 3 (STAT3) signaling pathway activation. Moreover, recombinant CIRP had no effect on cell proliferation or STAT3 phosphorylation but induced ER stress, which was blocked by TAK242, an inhibitor of Toll‑like receptor 4 (TLR4), in HepG2 cells. Taken together, the results of the present study demonstrated that intracellular CIRP promotes liver regeneration by activating the STAT3 pathway, whereas extracellular CIRP induces ER stress possibly via the TLR4 signaling pathway after hepatectomy.